Updated on 2025/10/23

写真a

 
OKAMURA Hirohiko
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Professor
Position
Professor
Homepage
https://hiro-okamura.wixsite.com/lab-oralmorphology
External link

Degree

  • 博士(歯学)

Research Interests

  • 細胞生物学

  • cell biology

Research Areas

  • Life Science / Oral biological science

Education

  • The University of Tokushima   歯学研究科  

    - 2004

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    Country： Japan

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  • Kyushu Dental College    

    - 1998

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  • Kyushu Dental College   歯学部   歯学科

    - 1998

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    Country： Japan

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Research History

  • 岡山大学・学術研究院医歯薬学域・教授

    2017.4

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  • 徳島大学・大学院医歯薬学研究部・准教授

    2015.4 - 2017.3

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  • 徳島大学・大学院医歯薬学研究部・助教

    2004.5 - 2015.3

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  • 日本学術振興会特別研究員

    2003.4 - 2004.4

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Professional Memberships

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Committee Memberships

  • 日本解剖学会   学術委員  

    2020.4   

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    Committee type：Academic society

  • Journal of Oral Biosciences   Associate Editor  

    2024.4   

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    Committee type：Academic society

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  • 日本解剖学会   第125回日本解剖学会総会・全国学術集会プログラム委員  

    2019.1 - 2020.12   

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    Committee type：Academic society

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  • 歯科基礎医学会   代議員  

    2018.5   

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    Committee type：Academic society

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  • 岡山歯学会   理事  

    2017.10   

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  • 日本解剖学会   評議員  

    2017.9   

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Papers

  • Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury. Reviewed

    Yishida K, Yoshida K, Fujiwara N, Seyama M, Ono K, Kawai H, Guo J, Wang Z, Weng Y, Yu Y, Uchida-Fukuhara Y, Ikegame M, Sasaki A, Nagatsuka H, Kamioka H, Okamura H, Ozaki K.

    Biochimica Biophysica Acta-Molecular Basis of Disease   1867 ( 11 )   166236   2021.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbadis.202

  • Gingipain regulates isoform switches of PD-L1 in macrophages infected with Porphyromonas gingivalis

    Yilin Zheng, Ziyi Wang, Yao Weng, Heriati Sitosari, Yuhan He, Xiu Zhang, Noriko Shiotsu, Yoko Fukuhara, Mika Ikegame, Hirohiko Okamura

    Scientific Reports   15 ( 1 )   2025.3

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    Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    DOI： 10.1038/s41598-025-94954-7

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    Other Link： https://www.nature.com/articles/s41598-025-94954-7

  • Angiogenin-induced Osteoclastogenesis Mediates Bone Destruction in Oral Squamous Carcinoma

    KASUMI AOKI, NANA YOSHITANI, NAITO KURIO, NORIE YOSHIOKA, JUMPEI TERAMACHI, MIKA IKEGAME, HIROHIKO OKAMURA, SOICHIRO IBARAGI

    Anticancer Research   45 ( 3 )   1025 - 1033   2025.3

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    Publishing type：Research paper (scientific journal)   Publisher：Anticancer Research USA Inc.  

    DOI： 10.21873/anticanres.17489

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  • PTPA localized in the Golgi apparatus plays an important role in osteoblast differentiation

    Xinyu Zheng, Yao Weng, Ayano Satoh, Airi Tanai, Mika Ikegame, Koji Kimura, Nana Yoshitani, Xiaohua Xie, Hirohiko Okamura

    Biochemical and Biophysical Research Communications   748   151329 - 151329   2025.2

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    Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.bbrc.2025.151329

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  • High Glucose Inhibits O‐GlcNAc Transferase Translocation in Early Osteoblast Differentiation by Altering Protein Phosphatase 2A Activity

    Heriati Sitosari, Yoko Fukuhara, Yao Weng, Yilin Zheng, Yuhan He, Xinyu Zheng, Mika Ikegame, Hirohiko Okamura

    Journal of Cellular Physiology   240 ( 1 )   2025.1

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    Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    ABSTRACT

    Our previous study revealed a link between O‐GlcNAc transferase (OGT) localization and protein phosphatase 2A (PP2A) activity in osteoblast. Given the association of PP2A downregulation with osteoblast differentiation, we hypothesized that OGT localization changes during this process. We examined OGT localization in MC3T3‐E1 cells undergoing differentiation under normal and high glucose conditions. Changes in PP2A activity were followed by alterations in OGT localization. Organ culture of calvaria revealed similar OGT localization changes in bone‐surrounding osteoblasts near the suture area. Furthermore, the levels of O‐GlcNAc modification in various proteins including Runt‐related transcription factor 2, Osterix, and ATP synthase subunit alpha (ATP5A) were shifted in parallel with OGT translocation. These findings suggest a regulatory role of OGT, under the influence of PP2A, during osteoblast differentiation.

    DOI： 10.1002/jcp.31524

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  • P. gingivalis-Infected Macrophage Extracellular Vesicles Cause Adverse Pregnancy Outcomes. International journal

    A Tanai, Y Fukuhara, T Eguchi, H Kawai, K Ueda, K Ochiai, M Ikegame, K Okamoto, H Okamura

    Journal of dental research   104 ( 1 )   54 - 63   2025.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    Periodontitis is a chronic inflammatory disease triggered by oral bacterial infection, with the bacterium Porphyromonas gingivalis being a major causative agent. The association between periodontitis and various systemic diseases has been demonstrated. Recent research has also highlighted the relationship between the aggravation of maternal periodontitis and adverse pregnancy outcomes such as preterm birth and low birth weight. However, the molecular mechanisms underlying how factors from periodontitis influence pregnancy and fetal development remain unclear. Extracellular vesicles (EVs) are nano-sized spherical particles secreted into the tissue microenvironment by various types of cells. EVs have garnered interest in recent years due to their role in intercellular communication. In the present study, we investigated whether EVs derived from P. gingivalis-infected macrophages (Pg-inf EVs) reach the feto-placental unit and influence fetal development. Through a series of in vivo experiments in mice, we demonstrated that Pg-inf EVs translocated to the feto-placental unit and impaired fetal development in size and weight. Histological analysis revealed disoriented blood vessel alignment and impaired angiogenesis in the placentas of Pg-inf EV-injected groups, indicative of compromised placental function. Proteome analysis revealed a significant decrease in Vegfr1 expression in the placentas of the experimental group. Moreover, Pg-inf EVs reduced VEGFR1 expression in cultured human vascular endothelial cells, highlighting a potential molecular mechanism through which these EVs exert their effects on placental angiogenesis. This is the first study to reveal a novel pathway in which oral bacteria-infected macrophage EVs in maternal periodontitis affect pregnancy via the feto-placental unit.

    DOI： 10.1177/00220345241285132

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  • O‐<scp>GlcNAcylation</scp> regulates osteoblast differentiation through the morphological changes in mitochondria, cytoskeleton, and endoplasmic reticulum Reviewed

    Yao Weng, Ziyi Wang, Heriati Sitosari, Mitsuaki Ono, Hirohiko Okamura, Toshitaka Oohashi

    BioFactors   2024.10

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    Authorship：Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    Abstract

    To explore the potential mechanisms which O‐linked‐N‐acetylglucosaminylation (O‐GlcNAcylation) regulates osteogenesis, a publicly RNA‐seq dataset was re‐analyzed with literature‐mining and showed the primary targets of O‐GlcNAcylation in osteoblasts are mitochondria/cytoskeleton. Although the O‐GlcNAcylation‐regulated mitochondria/cytoskeleton has been extensively studied, its specific role during osteogenesis remains unclear. To address this, we knocked out Ogt (Ogt‐KO) in MC3T3‐E1 osteoblastic cells. Then, significantly reduced osteoblast differentiation, motility, proliferation, mitochondria–endoplasmic reticulum (Mito–ER) coupling, volume of ER, nuclear tubulins, and oxygen metabolism were observed in Ogt‐KO cells. Through artificial intelligence (AI)‐predicted cellular structures, the time‐lapse live cells imaging with reactive‐oxygen‐species/hypoxia staining showed that lower cell proliferation and altered oxygen metabolism in the Ogt‐KO cells were correlated with the Mito–ER coupling. Bioinformatics analysis, combined with correlated mRNA and protein expression, suggested that Ezh2 and its downstream targets (Opa1, Gsk3a, Wnt3a, Hif1a, and Hspa9) may be involved in O‐GlcNAcylation‐regulated Mito–ER coupling, ultimately impacting osteoblast differentiation. In conclusion, our findings indicate that O‐GlcNAcylation‐regulated osteoblast differentiation is linked to morphological changes in mitochondria, cytoskeleton, and ER, with Ezh2 potentially playing a crucial role.

    DOI： 10.1002/biof.2131

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  • β-catenin binds to GSK-3β in liquid-liquid phase separation compartment in HEK293 cells Reviewed

    Kato M., Tanai A., Fukuhara Y., Zheng Y., Sitosari H., Yamamoto T., Ikegame M., Okamura H.

    Journal of Hard Tissue Biology   2024.10

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    Authorship：Corresponding author   Language：English  

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  • P. gingivalis-infected macrophage EVs cause adverse pregnancy outcomes Reviewed

    Tanai A., Fukuhara T., Eguchi T., Kawai K., Ueda K., Ochiai M., Ikegame M., Okamoto K., Okamura H.

    Journal of Dental Research   2024.9

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    Authorship：Corresponding author   Language：English  

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  • Mechanical stretching determines the orientation of osteoblast migration and cell division. Reviewed

    Fumiko Takemoto, Yoko Uchida-Fukuhara, Hiroshi Kamioka, Hirohiko Okamura, Mika Ikegame

    Anatomical science international   98 ( 4 )   521 - 528   2023.9

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    Osteoblasts alignment and migration are involved in the directional formation of bone matrix and bone remodeling. Many studies have demonstrated that mechanical stretching controls osteoblast morphology and alignment. However, little is known about its effects on osteoblast migration. Here, we investigated changes in the morphology and migration of preosteoblastic MC3T3-E1 cells after the removal of continuous or cyclic stretching. Actin staining and time-lapse recording were performed after stretching removal. The continuous and cyclic groups showed parallel and perpendicular alignment to the stretch direction, respectively. A more elongated cell morphology was observed in the cyclic group than in the continuous group. In both stretch groups, the cells migrated in a direction roughly consistent with the cell alignment. Compared to the other groups, the cells in the cyclic group showed an increased migration velocity and were almost divided in the same direction as the alignment. To summarize, our study showed that mechanical stretching changed cell alignment and morphology in osteoblasts, which affected the direction of migration and cell division, and velocity of migration. These results suggest that mechanical stimulation may modulate the direction of bone tissue formation by inducing the directional migration and cell division of osteoblasts.

    DOI： 10.1007/s12565-023-00716-8

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  • Neuropilin 1 (NRP1) Positively Regulates Adipogenic Differentiation in C3H10T1/2 Cells Reviewed International journal

    Yaqiong Yu, Yoko Uchida-Fukuhara, Yao Weng, Yuhan He, Mika Ikegame, Ziyi Wang, Kaya Yoshida, Hirohiko Okamura, Lihong Qiu

    International Journal of Molecular Sciences   24 ( 8 )   7394 - 7394   2023.4

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：MDPI AG  

    Neuropilin 1 (NRP1), a non-tyrosine kinase receptor for several ligands, is highly expressed in many kinds of mesenchymal stem cells (MSCs), but its function is poorly understood. In this study, we explored the roles of full-length NRP1 and glycosaminoglycan (GAG)-modifiable NRP1 in adipogenesis in C3H10T1/2 cells. The expression of full-length NRP1 and GAG-modifiable NRP1 increased during adipogenic differentiation in C3H10T1/2 cells. NRP1 knockdown repressed adipogenesis while decreasing the levels of Akt and ERK1/2 phosphorylation. Moreover, the scaffold protein JIP4 was involved in adipogenesis in C3H10T1/2 cells by interacting with NRP1. Furthermore, overexpression of non-GAG-modifiable NRP1 mutant (S612A) greatly promoted adipogenic differentiation, accompanied by upregulation of the phosphorylated Akt and ERK1/2. Taken together, these results indicate that NRP1 is a key regulator that promotes adipogenesis in C3H10T1/2 cells by interacting with JIP4 and activating the Akt and ERK1/2 pathway. Non-GAG-modifiable NRP1 mutant (S612A) accelerates the process of adipogenic differentiation, suggesting that GAG glycosylation is a negative post-translational modification of NRP1 in adipogenic differentiation.

    DOI： 10.3390/ijms24087394

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  • Inhibition of protein phosphatase 2A by okadaic acid induces translocation of nucleocytoplasmic O-GlcNAc transferase Reviewed International journal

    Heriati Sitosari, Ikkei Morimoto, Yao Weng, Yilin Zheng, Yoko Fukuhara, Mika Ikegame, Hirohiko Okamura

    Biochemical and Biophysical Research Communications   646   50 - 55   2023.2

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    Authorship：Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    Post-translational modification (PTM) is crucial for many biological events, such as the modulation of bone metabolism. Phosphorylation and O-GlcNAcylation are two examples of PTMs that can occur at the same site in the protein: serine and threonine residues. This phenomenon may cause crosstalk and possible interactions between the molecules involved. Protein phosphatase 2 A (PP2A) is widely expressed throughout the body and plays a major role in dephosphorylation. At the same location where PP2A acts, O-GlcNAc transferase (OGT) can introduce uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) molecules and mediates O-GlcNAc modifications. To examine the effects of PP2A inhibition on OGT localization and expression, osteoblastic MC3T3-E1 cells were treated with Okadaic Acid (OA), a potent PP2A inhibitor. In the control cells, OGT was strictly localized in the nucleus. However, OGT was observed diffusely in the cytoplasm of the OA-treated cells. This change in localization from the nucleus to the cytoplasm resulted from an increase in mitochondrial OGT expression and translocation of the nucleocytoplasmic isoform. Furthermore, knockdown of PP2A catalytic subunit α isoform (PP2A Cα) significantly affected OGT expression (p < 0.05), and there was a correlation between PP2A Cα and OGT expression (r = 0.93). These results suggested a possible interaction between PP2A and OGT, which strengthens the notion of an interaction between phosphorylation and O-GlcNAcylation.

    DOI： 10.1016/j.bbrc.2023.01.033

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  • Vestigial-Like 3 Plays an Important Role in Osteoblast Differentiation by Regulating the Expression of Osteogenic Transcription Factors and BMP Signaling. Reviewed International journal

    Haoze Yuan, Mika Ikegame, Yoko Fukuhara, Fumiko Takemoto, Yaqiong Yu, Jumpei Teramachi, Yao Weng, Jiajie Guo, Daisuke Yamada, Takeshi Takarada, Ying Li, Hirohiko Okamura, Bin Zhang

    Calcified tissue international   111 ( 3 )   331 - 344   2022.6

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    Our previous gene profiling analysis showed that the transcription cofactor vestigial-like 3 (VGLL3) gene expression was upregulated by mechanical tension in the mouse cranial suture, coinciding with accelerated osteoblast differentiation. Therefore, we hypothesized that VGLL3 plays a significant role in osteogenic differentiation. To clarify the function of VGLL3 in osteoblasts, we examined its expression characteristics in mouse bone tissue and the osteoblastic cell line MC3T3-E1. We further examined the effects of Vgll3 knockdown on osteoblast differentiation and bone morphogenetic protein (BMP) signaling. In the mouse cranial suture, where membranous ossification occurs, VGLL3 was immunohistochemically detected mostly in the nucleus of osteoblasts, preosteoblasts, and fibroblastic cells. VGLL3 expression in MC3T3-E1 cells was transient and peaked at a relatively early stage of differentiation. RNA sequencing revealed that downregulated genes in Vgll3-knockdown cells were enriched in gene ontology terms associated with osteoblast differentiation. Interestingly, most of the upregulated genes were related to cell division. Targeted Vgll3 knockdown markedly suppressed the expression of major osteogenic transcription factors (Runx2, Sp7/osterix, and Dlx5) and osteoblast differentiation. It also attenuated BMP signaling; moreover, exogenous BMP2 partially restore osteogenic transcription factors' expression in Vgll3-knockdown cells. Furthermore, overexpression of Vgll3 increased the expression of osteogenic transcription factors. These results suggest that VGLL3 plays a critical role in promoting osteoblast differentiation and that part of the process is mediated by BMP signaling. Further elucidation of VGLL3 function will increase our understanding of osteogenesis and skeletal disease etiology.

    DOI： 10.1007/s00223-022-00997-7

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  • Maternal Gut Microbiome Decelerates Fetal Endochondral Bone Formation by Inducing Inflammatory Reaction. Reviewed International journal

    Yoko Uchida-Fukuhara, Takako Hattori, Shanqi Fu, Sei Kondo, Miho Kuwahara, Daiki Fukuhara, Md Monirul Islam, Kota Kataoka, Daisuke Ekuni, Satoshi Kubota, Manabu Morita, Mika Iikegame, Hirohiko Okamura

    Microorganisms   10 ( 5 )   2022.5

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    To investigate the effect of the maternal gut microbiome on fetal endochondral bone formation, fetuses at embryonic day 18 were obtained from germ-free (GF) and specific-pathogen-free (SPF) pregnant mothers. Skeletal preparation of the fetuses' whole bodies did not show significant morphological alterations; however, micro-CT analysis of the tibiae showed a lower bone volume fraction in the SPF tibia. Primary cultured chondrocytes from fetal SPF rib cages showed a lower cell proliferation and lower accumulation of the extracellular matrix. RNA-sequencing analysis showed the induction of inflammation-associated genes such as the interleukin (IL) 17 receptor, IL 6, and immune-response genes in SPF chondrocytes. These data indicate that the maternal gut microbiome in SPF mice affects fetal embryonic endochondral ossification, possibly by changing the expression of genes related to inflammation and the immune response in fetal cartilage. The gut microbiome may modify endochondral ossification in the fetal chondrocytes passing through the placenta.

    DOI： 10.3390/microorganisms10051000

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  • Osteoblast Jmjd3 regulates osteoclastogenesis via EphB4 and RANKL signalling Reviewed

    Wang R, Luo H, Yang D, Yu B, Guo J, Shao L, Okamura H, Qiu L

    2022.2

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  • Histone Demethylase Jmjd3 Regulates the Osteogenic Differentiation and Cytokine Expressions of Periodontal Ligament Cells Reviewed

    Yu B, Wang R, Luo H, Yang D, Wang S, Yu Y, Okamura H, Qiu L

    Acta medica Okayama   76 ( 3 )   281 - 290   2022.1

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    Periodontal ligament (PDL) cells are critical for the bone remodeling process in periapical lesions since they can differentiate into osteoblasts and secrete osteoclastogenesis-promoting cytokines. Post-translational histone modifications including alterations of the methylation status of H3K27 are involved in cell differentiation and inflammatory reaction. The histone demethylase Jumonji domain-containing 3 (Jmjd3) specifically removes methylation of H3K27. We investigated whether Jmjd3 is involved in the osteogenic differentiation and secretion of PDL cells' inflammatory factors. Jmjd3 expression in periapical lesions was examined by immunostaining. Using siRNA specific for Jmjd3 or the specific Jmjd3 inhibitor GSK-J4, we determined Jmjd3's roles in osteogenic differentiation and cytokine production by real-time RT-PCR. The locations of Jmjd3 and NF-κB were analyzed by immunocytochemistry. Compared to healthy PDLs, the periapical lesion samples showed higher Jmjd3 expression. Treatment with GSK-J4 or Jmjd3 siRNA suppressed PDL cells' osteogenic differentiation by suppressing the expressions of bone-related genes (Runx2, Osterix, and osteocalcin) and mineralization. Jmjd3 knockdown decreased the expressions of cytokines (TNF-α, IL-1β, and IL-6) induced by lipopolysaccharide extracted from Porphyromonas endodontalis (Pe-LPS). Pe-LPS induced the nuclear translocations of Jmjd3 and NF-κB; the latter was inhibited by GSK-J4 treatment. Jmjd3 appears to regulate PDL cells' osteogenic differentiation and proinflammatory cytokine expressions.

    DOI： 10.18926/AMO/63722

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  • Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury. Reviewed International journal

    Kayo Yoshida, Kaya Yoshida, Natsumi Fujiwara, Mariko Seyama, Kisho Ono, Hotaka Kawai, Jiajie Guo, Ziyi Wang, Yao Weng, Yaqiong Yu, Yoko Uchida-Fukuhara, Mika Ikegame, Akira Sasaki, Hitoshi Nagatsuka, Hiroshi Kamioka, Hirohiko Okamura, Kazumi Ozaki

    Biochimica et biophysica acta. Molecular basis of disease   1867 ( 11 )   166236 - 166236   2021.11

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    Periodontal diseases are common inflammatory diseases that are induced by infection with periodontal bacteria such as Porphyromonas gingivalis (Pg). The association between periodontal diseases and many types of systemic diseases has been demonstrated; the term "periodontal medicine" is used to describe how periodontal infection/inflammation may impact extraoral health. However, the molecular mechanisms by which the factors produced in the oral cavity reach multiple distant organs and impact general health have not been elucidated. Extracellular vesicles (EVs) are nano-sized spherical structures secreted by various types of cells into the tissue microenvironment, and influence pathophysiological conditions by delivering their cargo. However, a detailed understanding of the effect of EVs on periodontal medicine is lacking. In this study, we investigated whether EVs derived from Pg-infected macrophages reach distant organs in mice and influence the pathophysiological status. EVs were isolated from human macrophages, THP-1 cells, infected with Pg. We observed that EVs from Pg-infected THP-1 cells (Pg-inf EVs) contained abundant core histone proteins such as histone H3 and translocated to the lungs, liver, and kidneys of mice. Pg-inf EVs also induced pulmonary injury, including edema, vascular congestion, inflammation, and collagen deposition causing alveoli destruction. The Pg-inf EVs or the recombinant histone H3 activated the NF-κB pathway, leading to increase in the levels of pro-inflammatory cytokines in human lung epithelial A549 cells. Our results suggest a possible mechanism by which EVs produced in periodontal diseases contribute to the progression of periodontal medicine.

    DOI： 10.1016/j.bbadis.2021.166236

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  • Outer membrane vesicles of Porphyromonas gingivalis: novel communication tool and strategy. Invited Reviewed International coauthorship

    Japanese Dental Science Review   57   138 - 146   2021.11

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    DOI： 10.1016/j.jdsr.2021.

  • Outer membrane vesicles of Porphyromonas gingivalis: Novel communication tool and strategy. Invited Reviewed International journal

    Hirohiko Okamura, Katsuhiko Hirota, Kaya Yoshida, Yao Weng, Yuhan He, Noriko Shiotsu, Mika Ikegame, Yoko Uchida-Fukuhara, Airi Tanai, Jiajie Guo

    The Japanese dental science review   57   138 - 146   2021.11

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    Extracellular vesicles (EVs) have been recognized as a universal method of cellular communications and are reportedly produced in bacteria, archaea, and eukaryotes. Bacterial EVs are often called "Outer Membrane Vesicles" (OMVs) as they were the result of a controlled blebbing of the outer membrane of gram-negative bacteria such as Porphyromonas gingivalis (P. gingivalis). Bacterial EVs are natural messengers, implicated in intra- and inter-species cell-to-cell communication among microorganism populations present in microbiota. Bacteria can incorporate their pathogens into OMVs; the content of OMVs differs, depending on the type of bacteria. The production of distinct types of OMVs can be mediated by different factors and routes. A recent study highlighted OMVs ability to carry crucial molecules implicated in immune modulation, and, nowadays, they are considered as a way to communicate and transfer messages from the bacteria to the host and vice versa. This review article focuses on the current understanding of OMVs produced from major oral bacteria, P. gingivalis: generation, characteristics, and contents as well as the involvement in signal transduction of host cells and systemic diseases. Our recent study regarding the action of P. gingivalis OMVs in the living body is also summarized.

    DOI： 10.1016/j.jdsr.2021.07.003

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  • Porphyromonas gingivalis impairs placental and fetal development through macrophage-derived extracellular vesicles) Reviewed

    2021   205 - 205   2021.10

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  • O‐GlcNAcylation drives calcium signaling toward osteoblast differentiation: A bioinformatics‐oriented study Reviewed

    Yao Weng, Ziyi Wang, Yoko Fukuhara, Airi Tanai, Mika Ikegame, Daisuke Yamada, Takeshi Takarada, Takashi Izawa, Satoru Hayano, Kaya Yoshida, Hiroshi Kamioka, Hirohiko Okamura

    BioFactors   2021.8

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    Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    DOI： 10.1002/biof.1774

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    Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/biof.1774

  • The role of extracellular vesicles throughout normal pregnancy and in relation to oral bacteria Reviewed

    Journal of Oral Biosciences   63 ( 1 )   14 - 22   2021.3

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.job.2021.01.006

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  • The role of extracellular vesicles throughout normal pregnancy and in relation to oral bacteria. Reviewed

    Tanai A, Okamura H.

    Journal of Oral Biosciences   63 ( 1 )   14 - 22   2021.1

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    Authorship：Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.job.2021.0

  • O-GlcNAcylation drives calcium signaling toward osteoblast differentiation: A bioinformatics-oriented study. Reviewed

    Weng Y, Wang Z, Fukuhara Y, Tanai A, Ikegame M, Yamada D, Takarada T, Izawa T, Hayano S, Yoshida K, Kamioka H, Okamura H.

    BioFactors   2021

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    Authorship：Last author,　Corresponding author   Language：English  

    DOI： 10.1002/biof.17

  • The inhibitory role of Rab11b in osteoclastogenesis through triggering lysosome-induced degradation of c-Fms and RANK surface receptors. Reviewed

    Tran MT, Okusha Y, Feng Y, Morimatsu M, Wei P, Sogawa C, Eguchi T, Kadowaki T, Sakai E, Okamura H, Naruse K, Tsukuba T, Okamoto K.

    International Journal of Molecular Sciences   21 ( 24 )   9352   2020.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.3390/ijms21249352

  • The Inhibitory Role of Rab11b in Osteoclastogenesis through Triggering Lysosome-Induced Degradation of c-Fms and RANK Surface Receptors Reviewed

    Manh Tien Tran, Yuka Okusha, Yunxia Feng, Masatoshi Morimatsu, Penggong Wei, Chiharu Sogawa, Takanori Eguchi, Tomoko Kadowaki, Eiko Sakai, Hirohiko Okamura, Keiji Naruse, Takayuki Tsukuba, Kuniaki Okamoto

    International Journal of Molecular Sciences   21 ( 24 )   9352 - 9352   2020.12

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    Publishing type：Research paper (scientific journal)   Publisher：MDPI AG  

    Rab11b, abundantly enriched in endocytic recycling compartments, is required for the establishment of the machinery of vesicle trafficking. Yet, no report has so far characterized the biological function of Rab11b in osteoclastogenesis. Using in vitro model of osteoclasts differentiated from murine macrophages like RAW-D cells or bone marrow-derived macrophages, we elucidated that Rab11b served as an inhibitory regulator of osteoclast differentiation sequentially via (i) abolishing surface abundance of RANK and c-Fms receptors; and (ii) attenuating nuclear factor of activated T-cells c1 (NFATc-1) upstream signaling cascades, following RANKL stimulation. Rab11b was localized in early and late endosomes, Golgi complex, and endoplasmic reticulum; moreover, its overexpression enlarged early and late endosomes. Upon inhibition of lysosomal function by a specific blocker, chloroquine (CLQ), we comprehensively clarified a novel function of lysosomes on mediating proteolytic degradation of c-Fms and RANK surface receptors, drastically ameliorated by Rab11b overexpression in RAW-D cell-derived osteoclasts. These findings highlight the key role of Rab11b as an inhibitor of osteoclastogenesis by directing the transport of c-Fms and RANK surface receptors to lysosomes for degradation via the axis of early endosomes-late endosomes-lysosomes, thereby contributing towards the systemic equilibrium of the bone resorption phase.

    DOI： 10.3390/ijms21249352

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  • Loading history changes the morphology and compressive force-induced expression of receptor activator of nuclear factor kappa B ligand/osteoprotegerin in MLO-Y4 osteocytes. Reviewed

    Wang Z, Weng Y, Ishihara Y, Odagaki N, Ei Hsu Hlaing E, Izawa T, Okamura H, Kamioka H.

    Peer J   8   e10244   2020.11

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    DOI： 10.7717/peerj.10244.

  • Loading history changes the morphology and compressive force-induced expression of receptor activator of nuclear factor kappa B ligand/osteoprotegerin in MLO-Y4 osteocytes Reviewed

    Ziyi Wang, Yao Weng, Yoshihito Ishihara, Naoya Odagaki, Ei Ei Hsu Hlaing, Takashi Izawa, Hirohiko Okamura, Hiroshi Kamioka

    PeerJ   8   e10244 - e10244   2020.11

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    <sec>
    <title>Background</title>
    In this study, we investigated the effect of the mechanical loading history on the expression of receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) in MLO-Y4 osteocyte-like cells.


    </sec>
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    Three hours after MLO-Y4 osteocytes were seeded, a continuous compressive force (CCF) of 31 dynes/cm2 with or without additional CCF (32 dynes/cm2) was loaded onto the osteocytes. After 36 h, the additional CCF (loading history) was removed for a recovery period of 10 h. The expression of RANKL, OPG, RANKL/OPG ratio, cell numbers, viability and morphology were time-dependently examined at 0, 3, 6 and 10 h. Then, the same additional CCF was applied again for 1 h to all osteocytes with or without the gap junction inhibitor to examine the expression of RANKL, OPG, the RANKL/OPG ratio and other genes that essential to characterize the phenotype of MLO-Y4 cells. Fluorescence recovery after photobleaching technique was also applied to test the differences of gap-junctional intercellular communications (GJIC) among MLO-Y4 cells.


    </sec>
    <sec>
    <title>Results</title>
    The expression of RANKL and OPG by MLO-Y4 osteocytes without a loading history was dramatically decreased and increased, respectively, in response to the 1-h loading of additional weight. However, the expression of RANKL, OPG and the RANKL/OPG ratio were maintained at the same level as in the control group in the MLO-Y4 osteocytes with a loading history but without gap junction inhibitor treatment. Treatment of loading history significantly changed the capacity of GJIC and protein expression of connexin 43 (Cx43) but not the mRNA expression of Cx43. No significant difference was observed in the cell number or viability between the MLO-Y4 osteocyte-like cells with and without a loading history or among different time checkpoints during the recovery period. The cell morphology showed significant changes and was correlated with the expression of OPG, Gja1 and Dmp1 during the recovery period.


    </sec>
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    <title>Conclusion</title>
    Our findings indicated that the compressive force-induced changes in the RANKL/OPG expression could be habituated within at least 11 h by 36-h CCF exposure. GJIC and cell morphology may play roles in response to loading history in MLO-Y4 osteocyte-like cells.


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  • N-(3-oxododecanoyl)-homoserine lactone regulates osteoblast apoptosis and differentiation by mediating intracellular calcium. Reviewed International coauthorship

    Guo J, Wang Z, Weng Y, Yuan H, Yoshida K, Ikegame M, Uchibe K, Kamioka H, Ochiai K, Okamura H, Qiu L.

    Cellular Signaling   75   1097450   2020.11

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    DOI： 10.1016/j.cellsig.20

  • Outer membrane vesicles derived from porphylomonas gingivalis induced cell death with disruption of tight junctions in human lung epithelial cells. Reviewed International coauthorship

    He Y, Shiotsu N, Uchida-Fukuhara Y, Guo J, Weng Y, Ikegame M, Wang Z, Ono K, Kamioka H, Torii Y, Sasaki A, Yoshida K, Okamura H.

    Archives of Oral Biology   118   104841   2020.10

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    DOI： 10.1016/j.archoralbi

  • Outer membrane vesicles derived from Porphyromonas gingivalis induced cell death with disruption of tight junctions in human lung epithelial cells. Reviewed International journal

    Archives of oral biology   118   104841 - 104841   2020.10

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    OBJECTIVE: Porphyromonas gingivalis (P. gingivalis) is a major bacterium responsible for the progression of periodontitis. P. gingivalis produces small vesicles called outer membrane vesicles (OMVs) containing virulence factors. Increasing evidence suggests a close relationship between periodontitis and respiratory system diseases, such as aspiration pneumonia. However, little is known about whether P. gingivalis OMVs give rise to the impediment of lung epithelial cells. We investigated the effect of the OMVs on cell viability and tight junctions of lung epithelial cells. DESIGN: Human lung epithelial A549 cells were treated with P. gingivalis OMVs. Cell viability was evaluated, and cell morphology was examined using scanning electron and phase contrast microscopies. To detect apoptosis induced by P. gingivalis OMVs, activation of caspase-3 and poly ADP-ribose polymerase (PARP) cleavage was examined by using Western blotting. Immunocytochemistry was performed to stain tight junction proteins. RESULTS: P. gingivalis OMVs decreased cell viability in A549 cells in a dose- and time-dependent manner. Microscopic analysis revealed that the OMVs induced morphological changes leading to irregular cell membrane structures. The OMVs caused cell shrinkage, membrane blebbing, and cytoplasmic expulsion in a dose-dependent manner. Western blot analysis showed the OMVs induced caspase-3 activation and PARP cleavage. Treatment with the OMVs disrupted the intact distributions of tight junction proteins. CONCLUSIONS: These results indicate that P. gingivalis OMVs induced cell death by destroying the barrier system in lung epithelial cells. Our present study raises the possibility that P. gingivalis OMVs is an important factor in the engagement of periodontitis with respiratory system diseases.

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  • N-(3-oxododecanoyl)-homoserine lactone regulates osteoblast apoptosis and differentiation by mediating intracellular calcium. Reviewed International journal

    Jiajie Guo, Ziyi Wang, Yao Weng, Haoze Yuan, Kaya Yoshida, Mika Ikegame, Kenta Uchibe, Hiroshi Kamioka, Kazuhiko Ochiai, Hirohiko Okamura, Lihong Qiu

    Cellular signalling   75   109740 - 109740   2020.8

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    Pseudomonas aeruginosa (P. aeruginosa) is associated with periapical periodontitis. The lesions are characterized by a disorder in osteoblast metabolism. Quorum sensing molecular N-(3-oxododecanoyl)-homoserine lactone (AHL) is secreted by P. aeruginosa and governs the expression of numerous virulence factors. AHL can trigger intracellular calcium ([Ca2+]i) fluctuations in many host cells. However, it is unclear whether AHL can regulate osteoblast metabolism by affecting [Ca2+]i changes or its spatial correlation. We explored AHL-induced apoptosis and differentiation in pre-osteoblastic MC3T3-E1 cells and evaluated [Ca2+]i mobilization using several extraction methods. The spatial distribution pattern of [Ca2+]i among cells was investigated by Moran's I, an index of spatial autocorrelation. We found that 30 μM and 50 μM AHL triggered opposing osteoblast fates. At 50 μM, AHL inhibited osteoblast differentiation by promoting mitochondrial-dependent apoptosis and negatively regulating osteogenic marker genes, including Runx2, Osterix, bone sialoprotein (Bsp), and osteocalcin (OCN). In contrast, prolonged treatment with 30 μM AHL promoted osteoblast differentiation concomitantly with cell apoptosis. The elevation of [Ca2+]i levels in osteoblasts treated with 50 μM AHL was spatially autocorrelated, while no such phenomenon was observed in 30 μM AHL-treated osteoblasts. The blocking of cell-to-cell spatial autocorrelation in the osteoblasts provoked by 50 μM AHL significantly inhibited apoptosis and partially restored differentiation. Our observations suggest that AHL affects the fate of osteoblasts (apoptosis and differentiation) by affecting the spatial correlation of [Ca2+]i changes. Thus, AHL acts as a double-edged sword for osteoblast function.

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  • Outer membrane vesicles of Porphyromonas gingivalis attenuate insulin sensitivity by delivering gingipains to the liver. Reviewed International coauthorship

    Seyama M, Yoshida K, Yoshida K, Fujiwara N, Ono K, Eguchi T, Kawai H, Guo J, Weng Y, Haoze Y, Uchibe K, Ikegame M, Sasaki A, Nagatsuka H, Okamoto K, Okamura H, Ozaki K.

    Biochimica Biophysica Acta-Molecular Basis of Disease   1866 ( 6 )   165731   2020.6

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    DOI： 10.1016/j.bbadis.202

  • Outer membrane vesicles of Porphyromonas gingivalis attenuate insulin sensitivity by delivering gingipains to the liver Reviewed

    Mariko Seyama, Kaya Yoshida, Kayo Yoshida, Natsumi Fujiwara, Kisho Ono, Takanori Eguchi, Hotaka Kawai, Jiajie Guo, Yao Weng, Yuan Haoze, Kenta Uchibe, Mika Ikegame, Akira Sasaki, Hitoshi Nagatsuka, Kuniaki Okamoto, Hirohiko Okamura, Kazumi Ozaki

    Biochimica et Biophysica Acta - Molecular Basis of Disease   1866 ( 6 )   2020.6

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  • Triple knockdown of CDC37, HSP90-alpha and HSP90-beta diminishes extracellular vesicles-driven malignancy events and macrophage M2 polarization in oral cancer.

    Ono K, Sogawa C, Kawai H, Tran HK, Taha EA, Lu Y, Oo MW, Okusha Y, Okamura H, Ibaragi S, Takigawa M, Kozaki K, Nagatsuka H, Sasaki A, Okamoto K, Calderwood SK, Eguchi T.

    Journal of Extracellular Vesicles   9 ( 1 )   1769373   2020.5

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    DOI： 10.1080/20013078.

  • Extracellular Vesicles Enriched with Moonlighting Metalloproteinase Are Highly Transmissive, Pro-Tumorigenic, and Trans-Activates Cellular Communication Network Factor Reviewed International coauthorship

    Okusha Y, Eguchi T, Tran MT, Sogawa C, Yoshida K, Itagaki M, Taha EA, Ono K, Aoyama E, Okamura H, Kozaki KI, Calderwood SK, Takigawa M, Okamoto K.

    Cancers (Basel)   12 ( 4 )   E881   2020.4

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    DOI： 10.3390/cancers12040

  • Extracellular Vesicles Enriched with Moonlighting Metalloproteinase Are Highly Transmissive, Pro-Tumorigenic, and Trans-Activates Cellular Communication Network Factor (CCN2/CTGF): CRISPR against Cancer Reviewed

    Yuka Okusha, Takanori Eguchi, Manh T. Tran, Chiharu Sogawa, Kaya Yoshida, Mami Itagaki, Eman A. Taha, Kisho Ono, Eriko Aoyama, Hirohiko Okamura, Ken-ichi Kozaki, Stuart K. Calderwood, Masaharu Takigawa, Kuniaki Okamoto

    Cancers   12 ( 4 )   881 - 881   2020.4

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    DOI： 10.3390/cancers12040881

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  • Extracellular Oncosomes Rich in Moonlighting Metalloproteinase (MMP3) Are Transmissive, Pro-Tumorigenic, and Induces Cellular Communication Network Factor 2 (CCN2/CTGF): CRISPR against Cancer

    Yuka Okusha, Takanori Eguchi, Manh Tien Tran, Chiharu Sogawa, Kaya Yoshida, Mami Itagaki, Eman Ahmed Taha, Kisho Ono, Eriko Aoyama, Hirohiko Okamura, Ken-ichi Kozaki, Stuart K. Calderwood, Masaharu Takigawa, Kuniaki Okamoto

    Preprints   doi: 10.20944/preprints202002.0281.v1   2020.2

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    Matrix metalloproteinase 3 (MMP3) plays multiple roles in pro-tumorigenic proteolysis and in intracellular transcription. These include inducing connective tissue growth factor [CTGF, also known as cellular communication network factor 2 (CCN2)] and prompting a new definition of MMP3 as a moonlighting metalloproteinase. Members of the MMP family have been found within tumor-derived extracellular vesicles (EVs) such as oncosomes or exosomes. We here investigated the roles of MMP3-rich oncosomes in tumor progression, molecular transmission, and gene regulation. MMP3 and CCN2/CTGF were significantly co-expressed in tumor samples derived from patients suffering from colorectal adenocarcinoma. We found that oncosomes derived from a rapidly metastatic colon cancer cells (LuM1) were enriched in MMP3 and a C-terminal half fragment of CCN2/CTGF. MMP3-rich oncosomes were highly transmissive into recipient cells and were pro-tumorigenic in an allograft mouse model. Oncosome-derived MMP3 was transmissive into recipient cell nuclei, trans-activated CCN2/CTGF promoter, and induced CCN2/CTGF production at 1 to 6 hours after the addition of oncosomes to culture media. In addition, CRISPR/Cas9-mediated knockout of MMP3 showed significant anti-tumor effects, including inhibition of migration and invasion of LuM1 cells in vitro, inhibition of tumor growth in vivo, and reduction of CCN2/CTGF and its promoter activity in vitro. These data newly demonstrate that the oncosome-derived moonlighting metalloproteinase promotes metastasis and is pro-tumorigenic at distant sites as well as a transmissive trans-activator for the cellular communication network gene.

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  • Triple knockdown of CDC37, HSP90-alpha and HSP90-beta diminishes extracellular vesicles-driven malignancy events and macrophage M2 polarization in oral cancer

    Kisho Ono, Chiharu Sogawa, Hotaka Kawai, Manh Tien Tran, Eman A. Taha, Yanyin Lu, May Wathone Oo, Yuka Okusha, Hirohiko Okamura, Soichiro Ibaragi, Masaharu Takigawa, Ken-Ichi Kozaki, Hitoshi Nagatsuka, Akira Sasaki, Kuniaki Okamoto, Stuart K. Calderwood, Takanori Eguchi

    Journal of Extracellular Vesicles   9 ( 1 )   1769373 - 1769373   2020.1

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  • Quorum-sensing molecule N-(3-Oxododecanoyl)-L-Homoserine lactone: An all-rounder in mammalian cell modification. Invited Reviewed International coauthorship

    Guo J, Yoshida K, Ikegame M, Okamura H.

    Journal of Oral Biosciences   62 ( 1 )   16 - 29   2020.1

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    DOI： 10.1016/j.job.2020.0

  • Inhibitory effect of retinoic acid receptor agonists on in vitro chondrogenic differentiation. Reviewed

    Sumitani Y, Uchibe K, Yoshida K, Weng Y, Guo J, Yuan H, Ikegame M, Kamioka H, Okamura H

    Anatomical Science International   2019

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  • Porphyromonas gingivalis感染したマクロファージが産生する膜小胞が肝臓糖代謝に及ぼす影響 Reviewed

    吉田 賀弥, 藤原 奈津美, 尾崎 和美, 内部 健太, 池亀 美華, 岡村 裕彦

    Journal of Oral Biosciences Supplement   2018   153 - 153   2018.9

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  • Expression of Noncollagenous Bone Matrix Proteins in Osteoblasts Stimulated by Mechanical Stretching in the Cranial Suture of Neonatal Mice. Reviewed

    Ikegame M, Ejiri S, Okamura H

    The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society   22155418793588   2018.8

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  • Reduction of protein phosphatase 2A Cα promotes in vivo bone formation and adipocyte differentiation. Reviewed International journal

    Kaya Yoshida, Jumpei Teramachi, Kenta Uchibe, Mika Ikegame, Lihong Qiu, Di Yang, Hirohiko Okamura

    Molecular and cellular endocrinology   470   251 - 258   2018.7

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    DOI： 10.1016/j.mce.2017.11.005

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  • Upregulated osterix expression elicited by Runx2 and Dlx5 is required for the accelerated osteoblast differentiation in PP2A Cα-knockdown cells Reviewed

    Di Yang, Hirohiko Okamura, Lihong Qiu

    Cell Biology International   42 ( 4 )   403 - 410   2018.4

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    DOI： 10.1002/cbin.10902

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  • Organoids with cancer stem cell-like properties secrete exosomes and HSP90 in a 3D nanoenvironment Reviewed

    Takanori Eguchi, Chiharu Sogawa, Yuka Okusha, Kenta Uchibe, Ryosuke Iinuma, Kisho Ono, Keisuke Nakano, Jun Murakami, Manabu Itoh, Kazuya Arai, Toshifumi Fujiwara, Yuri Namba, Yoshiki Murata, Kazumi Ohyama, Manami Shimomura, Hirohiko Okamura, Masaharu Takigawa, Tetsuya Nakatsura, Ken-ichi Kozaki, Kuniaki Okamoto, Stuart K. Calderwood

    PLoS ONE   13 ( 2 )   e0191109   2018.2

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  • 多彩な役割をもつ蛋白質脱リン酸化酵素PP2A Invited Reviewed

    岡村 裕彦

    岡山歯学会雑誌   36 ( 2 )   25 - 36   2018

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  • PKR induces the expression of NLRP3 by regulating the NF-κB pathway in Porphyromonas gingivalis-infected osteoblasts Reviewed

    Kaya Yoshida, Hirohiko Okamura, Yuka Hiroshima, Kaori Abe, Jun-ichi Kido, Yasuo Shinohara, Kazumi Ozaki

    Experimental Cell Research   Vol.354 ( No.1 )   57 - 64   2017.5

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    The double-stranded RNA-dependent kinase (PKR), which is activated by double stranded RNA, induces inflammation by regulating NF-κB signaling. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome also modulates inflammation in response to infection. Porphyromonas gingivalis (P.gingivalis) is an oral bacterium which is implicated in the pathogenesis of periodontal diseases. We previously reported that PKR is a key modulator of bone metabolism and inflammation in the periodontal tissue. PKR was also reported to induce inflammation in response to microbes by regulating the NLRP3 inflammasome, suggesting that PKR could affect inflammation along with NLRP3 in periodontal diseases. In this study, we investigated the effects of PKR on NLRP3 expression and NF-κB activity in P. gingivalis infected osteoblasts. We first constructed a SNAP26b-tagged P.gingivalis (SNAP-P. g.) and traced its internalization into the cell. SNAP-P. g. increased the activity of PKR and NF-κB and also induced NLRP3 expression in osteoblasts. Inhibition of NF-κB attenuated SNAP-P. g.-induced NLRP3 expression. The knockdown of PKR using shRNA decreased both the activity of NF-κB and the expression of NLRP3 induced by SNAP-P.g.. We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 expression by activating NF-κB. Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 inflammasome through the NF-κB pathway in periodontal diseases.

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  • PKR induces the expression of NLRP3 by regulating the NF-kappa B pathway in Porphyromonas gingivalis-infected osteoblasts Reviewed

    Kaya Yoshida, Hirohiko Okamura, Yuka Hiroshima, Kaori Abe, Jun-ichi Kido, Yasuo Shinohara, Kazumi Ozaki

    EXPERIMENTAL CELL RESEARCH   354 ( 1 )   57 - 64   2017.5

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  • Role of Protein Phosphatase 2A in Osteoblast Differentiation and Function Reviewed

    Hirohiko Okamura, Kaya Yoshida, Hiroyuki Morimoto, Jumpei Teramachi, Kazuhiko Ochiai, Tatsuji Haneji, Akihito Yamamoto

    JOURNAL OF CLINICAL MEDICINE   6 ( 3 )   2017.3

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  • PKR regulates LPS-induced osteoclast formation and bone destruction in vitro and in vivo Reviewed

    J. Teramachi, Y. Inagaki, H. Shinohara, H. Okamura, D. Yang, K. Ochiai, R. Baba, H. Morimoto, T. Nagata, T. Haneji

    ORAL DISEASES   23 ( 2 )   181 - 188   2017.3

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  • Involvement of interleukin-23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis Reviewed

    Nan Ma, Di Yang, Hirohiko Okamura, Jumpei Teramachi, Tomokazu Hasegawa, Lihong Qiu, Tatsuji Haneji

    MOLECULAR MEDICINE REPORTS   15 ( 2 )   559 - 566   2017.2

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  • Protein phosphatase 2A C alpha regulates proliferation, migration, and metastasis of osteosarcoma cells Reviewed

    Di Yang, Hirohiko Okamura, Hiroyuki Morimoto, Jumpei Teramachi, Tatsuji Haneji

    LABORATORY INVESTIGATION   96 ( 10 )   1050 - 1062   2016.10

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  • Porphyromonas gingivalis attenuates the insulin-induced phosphorylation and translocation of forkhead box protein O1 in human hepatocytes Reviewed

    Haruna Takamura, Kaya Yoshida, Hirohiko Okamura, Natsumi Fujiwara, Kazumi Ozaki

    ARCHIVES OF ORAL BIOLOGY   69   19 - 24   2016.9

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  • Histone demethylase Jmjd3 regulates osteoblast apoptosis through targeting anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bim. Reviewed International journal

    Di Yang, Hirohiko Okamura, Jumpei Teramachi, Tatsuji Haneji

    Biochimica et biophysica acta   1863 ( 4 )   650 - 9   2016.4

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    Posttranslational modifications including histone methylation regulate gene transcription through directly affecting the structure of chromatin. Trimethylation of histone H3K27 (H3K27me3) contributes to gene silencing and the histone demethylase Jumonji domain-containing 3 (Jmjd3) specifically removes the methylation of H3K27me3, followed by the activation of gene expression. In the present study, we explored the roles of Jmjd3 in regulating osteoblast apoptosis. Knockdown of Jmjd3 promoted osteoblast apoptosis induced by serum deprivation with decreased mitochondrial membrane potential and increased levels of caspase-3 activation, PARP cleavage, and DNA fragmentation. B cell lymphoma-2 (Bcl-2), an anti-apoptotic protein, was down-regulated by knockdown of Jmjd3 through retaining H3K27me3 on its promoter region. Knockdown of Jmjd3 increased the pro-apoptotic activity of Bim through inhibiting ERK-dependent phosphorylation of Bim. Protein kinase D1 (PKD1), which stimulates ERK phosphorylation, decreased in the Jmjd3-knockdown cells and introduction of PKD1 relieved osteoblast apoptosis in the Jmjd3-knockdown cells through increasing ERK-regulated Bim phosphorylation. These results suggest that Jmjd3 regulates osteoblast apoptosis through targeting Bcl-2 expression and Bim phosphorylation.

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  • Histone demethylase Jmjd3 regulates osteoblast apoptosis through targeting anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bim Reviewed

    Di Yang, Hirohiko Okamura, Jumpei Teramachi, Tatsuji Haneji

    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH   1863 ( 4 )   650 - 659   2016.4

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  • PKR regulates LPS-induced osteoclast formation and bone destruction in vitro and in vivo. Reviewed

    Jumpei Teramachi, Yuji Inagaki, Hiroki Shinohara, Hirohiko Okamura, Di Yang, Kazuhiko Ochiai, Ryoko Baba, Hiroyuki Morimoto, Toshihiko Nagata, Tatsuji Haneji

    Oral Diseases   2016

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    PKR plays a pivotal role in LPS-induced bone loss in PD, and, thus, has potential as a therapeutic target for PD. This article is protected by copyright. All rights reserved.

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  • Histone Demethylase Utx Regulates Differentiation and Mineralization in Osteoblasts Reviewed

    Di Yang, Hirohiko Okamura, Jumpei Teramachi, Tatsuji Haneji

    JOURNAL OF CELLULAR BIOCHEMISTRY   116 ( 11 )   2628 - 2636   2015.11

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  • Double Stranded RNA-Dependent Protein Kinase is Necessary for TNF--Induced Osteoclast Formation In Vitro and In Vivo Reviewed

    Hiroki Shinohara, Jumpei Teramachi, Hirohiko Okamura, Di Yang, Toshihiko Nagata, Tatsuji Haneji

    JOURNAL OF CELLULAR BIOCHEMISTRY   116 ( 9 )   1957 - 1967   2015.9

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  • Preventive Effect of Daiokanzoto (TJ-84) on 5-Fluorouracil-Induced Human Gingival Cell Death through the Inhibition of Reactive Oxygen Species Production Reviewed

    Kaya Yoshida, Masami Yoshioka, Hirohiko Okamura, Satomi Moriyama, Kazuyoshi Kawazoe, Daniel Grenier, Daisuke Hinode

    PLOS ONE   9 ( 11 )   e112689   2014.11

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  • Reduction of PP2A Cα stimulates adipogenesis by regulating the Wnt/GSK-3β/β-catenin pathway and PPARγ expression. Reviewed International journal

    Hirohiko Okamura, Di Yang, Kaya Yoshida, Jumpei Teramachi, Tatsuji Haneji

    Biochimica et biophysica acta   1843 ( 11 )   2376 - 84   2014.11

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    Serine/threonine protein phosphatase 2A (PP2A) regulates several physiological processes such as the cell cycle, cell growth, apoptosis, and signal transduction. In this study, we examined the expression and role of PP2A Cα in adipocyte differentiation. PP2A Cα expression and PP2A activity decreased during adipocyte differentiation in C3H10T1/2 and 3T3-L1 cells and the expression of adipocyte marker genes such as PPARγ and adiponectin increased. To further clarify the role of PP2A Cα in adipocyte differentiation, we constructed PP2A knockdown cells by infecting C3H10T1/2 cells with a lentivirus expressing a shRNA specific for the PP2A Cα (shPP2A cells). Silencing of PP2A Cα in C3H10T1/2 cells dramatically stimulated adipocyte differentiation and lipid accumulation, which were accompanied by expression of adipocyte marker genes. Silencing of PP2A Cα suppressed Wnt10b expression and reduced the levels of the inactivated form of GSK-3β (phospho-GSK-3β), leading to the reduction of β-catenin levels in the nucleus and its transcriptional activity. Treatment with LiCl, a GSK-3β inhibitor, and inhibition of PPARγ expression suppressed the accelerated adipogenesis of shPP2A cells. Our data indicate that PP2A Cα plays an important role in the regulation of adipocyte differentiation by regulating the Wnt/GSK-3β/β-catenin pathway and PPARγ expression.

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  • Reduction of PP2A C alpha stimulates adipogenesis by regulating the Wnt/GSK-3 beta/beta-catenin pathway and PPAR gamma expression Reviewed

    Hirohiko Okamura, Di Yang, Kaya Yoshida, Jumpei Teramachi, Tatsuji Haneji

    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH   1843 ( 11 )   2376 - 2384   2014.11

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  • Tumor necrosis factor-alpha induces interleukin-34 expression through nuclear factor-kappa B activation in MC3T3-E1 osteoblastic cells Reviewed

    Yaqiong Yu, Di Yang, Lihong Qiu, Hirohiko Okamura, Jiajie Guo, Tatsuji Haneji

    MOLECULAR MEDICINE REPORTS   10 ( 3 )   1371 - 1376   2014.9

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  • Calcium Hydroxide Suppresses Porphyromonas endodontalis Lipopolysaccharide-induced Bone Destruction Reviewed

    J. Guo, D. Yang, H. Okamura, J. Teramachi, K. Ochiai, L. Qiu, T. Haneji

    JOURNAL OF DENTAL RESEARCH   93 ( 5 )   508 - 513   2014.5

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  • Oral Porphyromonas gingivalis translocates to the liver and regulates hepatic glycogen synthesis through the Akt/GSK-3β signaling pathway. Reviewed International journal

    Makoto Ishikawa, Kaya Yoshida, Hirohiko Okamura, Kazuhiko Ochiai, Haruna Takamura, Natsumi Fujiwara, Kazumi Ozaki

    Biochimica et biophysica acta   1832 ( 12 )   2035 - 43   2013.12

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    Periodontal diseases are common chronic inflammatory disorders that result in the destruction of tissues around teeth. Many clinical studies suggest that periodontal diseases are risk factors for insulin resistance and diabetic mellitus development. However, the molecular mechanisms by which periodontal diseases regulate the progress of diabetes mellitus remain unknown. In this study, we investigated whether Porphyromonas gingivalis (P.g.), a major pathogen of periodontal diseases, present in the oral cavity, moves to the liver and affects hepatic glycogen synthesis. SNAP26b-tagged P.g. (SNAP-P.g.) was introduced into the oral cavity to induce periodontal disease in 4-week old female Balb/c mice. SNAP-P.g. was detected in the liver extracted from SNAP-P.g.-treated mice using nested PCR analysis. High blood glucose levels tended to promote SNAP-P.g. translocation from the oral cavity to the liver in mice. Periodic acid-Schiff staining suggested that hepatic glycogen synthesis decreased in SNAP-P.g.-treated mice. SNAP-P.g. was also internalized into the human hepatoma cell line HepG2, and this attenuated the phosphorylation of insulin receptor substrate (IRS)-1, Akt and glycogen synthase kinase-3β induced by insulin. Insulin-induced glycogen synthesis was suppressed by SNAP-P.g. in HepG2 cells. Our results suggest that P.g. translocation from the oral cavity to the liver may contribute to the progress of diabetes mellitus by influencing hepatic glycogenesis.

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  • Oral porphyromonas gingivalis translocates to the liver and regulates hepatic glycogen synthesis through the Akt/GSK-3b signaling pathway Reviewed

    Ishikawa Makoto, Kaya Yoshida, Hirohiko Okamura, Kazuhiko Ochiai, Takamura Haruna, Natsumi Fujiwara, Kazumi Ozaki

    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease   Vol.1832 ( No.12 )   2035 - 2043   2013.12

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    Periodontal diseases are common chronic inflammatory disorders that result in the destruction of tissues around teeth. Many clinical studies suggest that periodontal diseases are risk factors for insulin resistance and diabetic mellitus development. However, the molecular mechanisms by which periodontal diseases regulate the progress of diabetes mellitus remain unknown. In this study, we investigated whether Porphyromonas gingivalis (P.g.), a major pathogen of periodontal diseases, present in the oral cavity, moves to the liver and affects hepatic glycogen synthesis. SNAP26b-tagged P.g. (SNAP-P.g.) was introduced into the oral cavity to induce periodontal disease in 4-week old female Balb/c mice. SNAP-P.g. was detected in the liver extracted from SNAP-P.g.-treated mice using nested PCR analysis. High blood glucose levels tended to promote SNAP-P.g. translocation from the oral cavity to the liver in mice. Periodic acid-Schiff staining suggested that hepatic glycogen synthesis decreased in SNAP-P.g.-treated mice. SNAP-P.g. was also internalized into the human hepatoma cell line HepG2, and this attenuated the phosphorylation of insulin receptor substrate (IRS)-1, Akt and glycogen synthase kinase-3β induced by insulin. Insulin-induced glycogen synthesis was suppressed by SNAP-P.g. in HepG2 cells. Our results suggest that P.g. translocation from the oral cavity to the liver may contribute to the progress of diabetes mellitus by influencing hepatic glycogenesis.

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  • Histone Demethylase Jmjd3 Regulates Osteoblast Differentiation via Transcription Factors Runx2 and Osterix Reviewed

    Di Yang, Hirohiko Okamura, Yoshiki Nakashima, Tatsuji Haneji

    JOURNAL OF BIOLOGICAL CHEMISTRY   288 ( 47 )   33530 - 33541   2013.11

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  • Protein phosphatase 2A C alpha regulates osteoblast differentiation and the expressions of bone sialoprotein and osteocalcin via osterix transcription factor Reviewed

    Hirohiko Okamura, Kaya Yoshida, Di Yang, Tatsuji Haneji

    JOURNAL OF CELLULAR PHYSIOLOGY   228 ( 5 )   1031 - 1037   2013.5

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  • Protein phosphatase 2A Cα regulates osteoblast differentiation and the expressions of bone sialoprotein and osteocalcin via osterix transcription factor. Reviewed

    Hirohiko Okamura, Kaya Yoshida, Di Yang, Tatsuji Haneji

    Journal of Cellular Physiology   Vol.228 ( No.5 )   1031 - 1037   2013.5

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    Serine/threonine protein phosphatase 2A (PP2A) participates in regulating many important physiological processes such as cell cycle, growth, apoptosis, and signal transduction. Osterix is a zinc-finger-containing transcription factor that is essential for osteoblast differentiation and regulation of many bone-related genes. We have recently reported that decrease in α-isoform of PP2A catalytic subunit (PP2A Cα) accelerates osteoblast differentiation through the expression of bone-related genes. In this study, we further examined the role of PP2A Cα in osteoblast differentiation by establishing the stable cell lines that overexpress PP2A Cα. Overexpression of PP2A Cα reduced alkaline phosphatase (ALP) activity. Osteoblast differentiation and mineralization were also decreased in PP2A Cα-overexpressing cells, with reduction of bone-related genes including osterix, bone sialoprotein (Bsp), and osteocalcin (OCN). Luciferase assay showed that the transcriptional activity of the Osterix promoter region was decreased in PP2A Cα-overexpressing cells. Introduction of ectopic Osterix rescued the expression of Bsp and OCN in PP2A Cα-overexpressing cells. These results indicate that PP2A Cα and its activity play a negative role in osteoblast differentiation and Osterix is a key factor responsible for regulating the expressions of Bsp and OCN during PP2A Cα-mediated osteoblast differentiation.

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  • Protein phosphatase 2A C is involved in osteoclastogenesis by regulating RANKL and OPG expression in osteoblasts. Reviewed

    Hirohiko Okamura, Di Yang, Kaya Yoshida, Tatsuji Haneji

    FEBS Letters   Vol.587 ( No.1 )   48 - 53   2013.1

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    We examined whether alteration of PP2A Cα expression in osteoblasts is involved in osteoclast differentiation. Reduction of PP2A Cα in MC3T3-E1 cells (shPP2A) decreased receptor activator of nuclear factor κB ligand (RANKL) expression and increased osteoprotegerin (OPG) expression. The conditioned medium from shPP2A cells failed to induce NFATc1 as well as the expression of osteoclast marker genes cathepsin K and osteoclast-associated receptor (OSCAR) in bone marrow macrophage cells. Treatment of bone marrow macrophage cells with the conditioned medium from shPP2A cells impaired osteoclastogenesis. These results suggest that alteration of PP2A Cα expression in osteoblasts modulates the expressions of RANKL and OPG, which are involved in osteoclastogenesis via the NFATc1 transcription factor.

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  • Protein phosphatase 2A C alpha is involved in osteoclastogenesis by regulating RANKL and OPG expression in osteoblasts Reviewed

    Hirohiko Okamura, Di Yang, Kaya Yoshida, Tatsuji Haneji

    FEBS LETTERS   587 ( 1 )   48 - 53   2013.1

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  • PKR plays a positive role in osteoblast differentiation by regulating GSK-3β activity through a β-catenin-independent pathway Reviewed

    Kaya Yoshida, Hirohiko Okamura, Kazuhiko Ochiai, Yumi Hoshino, Tatsuji Haneji, Masami Yoshioka, Daisuke Hinode, Hideo Yoshida

    Molecular and Cellular Endocrinology   361 ( 1-2 )   99 - 105   2012.9

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  • PKR plays a positive role in osteoblast differentiation by regulating GSK-3b activity through a b-catenin-independent pathway Reviewed

    Kaya Yoshida, Hirohiko Okamura, Kazuhiko Ochiai, Yumi Hoshimo, Tatsuji Haneji, Masami Yoshioka, Daisuke Hinode, Hideo Yoshida

    Molecular and Cellular Endocrinology   Vol.361 ( No.1-2 )   99 - 105   2012.9

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    Double-stranded RNA-dependent protein kinase (PKR) is involved in various cellular functions. We previously reported that PKR regulates osteoblast differentiation, but the specific mechanisms by which this occurs remain unclear. In this study, we investigated the role of PKR in Glycogen synthase kinase 3 (GSK-3) regulation of osteoblast differentiation. Lithium chloride (LiCl), a GSK-3 inhibitor, increased GSK-3 phosphorylation in MC3T3-E1 and MG-63 cells. LiCl also inhibited Runx2 and expression of its regulated genes, causing inhibition of Alkaline phosphatase activity and mineralization. LiCl injection to the calvaria in mice suppressed bone formation. Further, GSK-3 phosphorylation was increased in osteoblasts, by Akt-independent mechanisms, in which PKR was constitutively inactivated. A PKR inhibitor, 2-aminopurine, also induced GSK-3 phosphorylation in MC3T3-E1 and MG-63 cells. Further, Runx2 and its regulated genes were inhibited in PKR-inactivated osteoblasts, and differentiation was suppressed through a -catenin-independent pathway. PKR positively regulates the differentiation of osteoblasts by mediating GSK-3 activity through a -catenin-independent pathway.

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  • Interaction between PKR and PACT mediated by LPS-inducible NF-?B in human gingival cells Reviewed

    Kaya Yoshida, Hirohiko Okamura, Yumi Hoshino, Masayuki Shono, Masami Yoshioka, Daisuke Hinode, Hideo Yoshida

    JOURNAL OF CELLULAR BIOCHEMISTRY   113 ( 1 )   165 - 173   2012.1

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  • Interaction between PKR and PACT mediated by LPS-inducible NF-kB in human gingival cells Reviewed

    Kaya Yoshida, Hirohiko Okamura, Yumi Hoshimo, Masayuki Shono, Masami Yoshioka, Daisuke Hinode, Hideo Yoshida

    Journal of Cellular Biochemistry   Vol.113   165 - 173   2012.1

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    The double-stranded RNA-dependent protein kinase (PKR) is a serine/threonine kinase expressed constitutively in mammalian cells. PKR is activated upon virus infection by double-stranded RNA (dsRNA), and plays a critical role in host antiviral defense mechanisms. PKR is also known to regulate various biological responses, including cell differentiation and apoptosis. However, whether PKR is involved in the progress of periodontitis is not clear. The present study explained the phosphorylation of PKR by LPS in the human gingival cell line, Sa3. Expression of genes encoding LPS receptors was detected in Sa3 cells and treatment of cells with 1 μg/mL LPS for 6 h caused PKR phosphorylation. LPS elevated the expression of the protein activator of PKR (PACT) mRNA and protein, followed by the enhanced association between PACT and PKR within 3 h. In addition, LPS treatment induced the translocation of NF-κB to the nucleus after 30 min, and inhibition of NF-κB decreased the PACT-PKR interaction induced by LPS. The level of pro-inflammatory cytokine mRNA, including interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFα), appeared within 45 min and reached at the maximal levels by 90 min after the addition of LPS. This induction of pro-inflammatory cytokines was not affected by RNAi-mediated silencing of PKR and a pharmacological inhibitor of PKR, whereas the inhibition of NF-κB decreased it. These results indicated that LPS induces PKR phosphorylation and the PACT-PKR association in Sa3 cells. Our results also suggest that NF-κB is involved in the PACT-PKR interaction and the production of pro-inflammatory cytokines in periodontitis.

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  • Reduction of protein phosphatase 2A C alpha enhances bone formation and osteoblast differentiation through the expression of bone-specific transcription factor Osterix Reviewed

    Hirohiko Okamura, Kaya Yoshida, Kazuhiko Ochiai, Tatsuji Haneji

    BONE   49 ( 3 )   368 - 375   2011.9

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  • Reduction of protein phosphatase 2A Cα enhances bone formation and osteoblast differentiation through the expression of bone-specific transcription factor Osterix. Reviewed

    Hirohiko Okamura, Kaya Yoshida, Kazuhiko Ochiai, Tatsuji Haneji

    Bone   Vol.49 ( No.3 )   368 - 375   2011.6

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    The serine/threonine protein phosphatase 2A (PP2A) participates in regulating many important physiological processes such as control of cell cycle, growth, and division. On the other hand, Osterix is a zinc-finger-containing transcription factor that is essential for the differentiation of osteoblasts and regulation of many bone-related genes. Here we examined the effect of okadaic acid (OA), a specific inhibitor of PP2A, on bone formation in vivo and the molecular mechanism regulated by PP2A Cα in osteoblast differentiation. Administration of 1nM OA to the calvarial region in mice increased bone mineral density, as shown by μCT, while histomorphological analysis showed an increase in mineral apposition and bone thickness in the same region. In addition, treatment with 1nM OA stimulated osteoblast differentiation and the expression of Osterix, bone sialoprotein (Bsp), and osteocalcin (OCN) in mouse osteoblastic MC3T3-E1 cells. Moreover, the expression and phosphatase activity of PP2A Cα was decreased in the initial step of osteoblast differentiation, which was in parallel with an increase in Osterix expression. To further clarify the role of PP2A Cα in osteoblast differentiation, we constructed PP2A knock-down cells by infecting MC3T3-E1 cells with a lentivirus expressing shRNA specific for the PP2A Cα. Accordingly, the silencing of PP2A Cα in MC3T3-E1 cells dramatically increased osteoblast differentiation and mineralization, which were accompanied with expressions of Osterix, Bsp, and OCN. Our data indicate that PP2A Cα plays an important role in the regulation of bone formation and osteoblast differentiation through the bone-related genes.

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  • Intermedilysin induces EGR-1 expression through calcineurin/NFAT pathway in human cholangiocellular carcinoma cells Reviewed

    Heni Susilowati, Hirohiko Okamura, Katsuhiko Hirota, Masayuki Shono, Kaya Yoshida, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Tatsuji Haneji, Yoichiro Miyake

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   404 ( 1 )   57 - 61   2011.1

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  • Intermedilysin induces EGR-1 expression through calcineurin/NFAT pathway in human cholangiocellular carcinoma cells. Reviewed

    Heni Susilowati, Hirohiko Okamura, Katsuhiko Hirota, Masayuki Shono, Kaya Yoshida, Keiji Murakami, Atsushi Tabata, Hideaki Nagamune, Tatsuji Haneji, Yoichiro Miyake

    Biochemical and Biophysical Research Communications   Vol.404 ( No.1 )   57 - 61   2011

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    (Intermedilysin (ILY) is a cholesterol-dependent cytolysin produced by Streptococcus intermedius, which is associated with human brain and liver abscesses. Although intrahepatic bile duct cells play a valuable role in the pathogenesis of liver abscess, the molecular mechanism of ILY-treated intrahepatic bile duct cells remains unknown. In this study, we report that ILY induced a nuclear accumulation of intracellular calcium ([Ca(2+)]i) in human cholangiocellular cells HuCCT1. We also demonstrate that 10 ng/ml ILY induced NFAT1 dephosphorylation and its nuclear translocation in HuCCT1 cells. In contrast to the result that ILY induced NF-B translocation in human hepatic HepG2 cells, ILY did not affect NF-B localization in HuCCT1 cells. Dephosphorylation and nuclear translocation of NFAT1 caused by ILY were prevented by [Ca(2+)]i calcium chelator, BAPTA/AM, and calcineurin inhibitors, cyclosporine A and tacrolimus. ILY induced early growth response-1 (EGR-1) expression and it was inhibited by the pre-treatment with cyclosporine A, indicating that the calcineurin/NFAT pathway was involved in EGR-1 expression in response to ILY. ILY-induced calcineurin/NFAT1 activation and sequential EGR-1 expression might be related to the pathogenesis of S. intermedius in human bile duct cells.)

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  • Negative regulation of TIMP1 is mediated by transcription factor TWIST1 Reviewed

    Hirohiko Okamura, Kaya Yoshida, Tatsuji Haneji

    INTERNATIONAL JOURNAL OF ONCOLOGY   35 ( 1 )   181 - 186   2009.7

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  • PKR-mediated degradation of STAT1 regulates osteoblast differentiation Reviewed

    Kaya Yoshida, Hirohiko Okamura, Bruna Rabelo Amorim, Daisuke Hinode, Hideo Yoshida, Tatsuji Haneji

    EXPERIMENTAL CELL RESEARCH   315 ( 12 )   2105 - 2114   2009.7

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  • PKR-mediated degradation of STAT1 regulates osteoblast differentiation Reviewed

    Kaya Yoshida, Hirohiko Okamura, Bruna Rabelo Amorim, Daisuke Hinode, Hideo Yoshida, Tatsuji Haneji

    Experimental Cell Research   Vol.315 ( No.12 )   2105 - 2114   2009.7

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    The double-stranded RNA-dependent protein kinase (PKR) plays a critical role in various biological responses including antiviral defense, cell differentiation, apoptosis, and tumorigenesis. In this study, we investigated whether PKR could affect the post-translational modifications of STAT1 protein and whether these modifications regulate osteoblast differentiation. We demonstrated that PKR was necessary for the ubiquitination of STAT1 protein. The expressions of bone-related genes such as type I collagen, integrin binding sialoprotein, osteopontin, and osterix were suppressed in osteoblasts lacking PKR activity. In contrast, the expressions of interleukin-6 and matrix metalloproteinases 8 and 13 increased in PKR-mutated osteoblasts. The expression and degradation of STAT1 protein were regulated by PKR in a SLIM-dependent pathway. Inhibition of SLIM by RNA interference resulted in the decreased activity of Runx2 in osteoblasts. Stimulation of interleukin-6 expression and suppression of alkaline phosphatase activity were regulated through by SLIM-dependent pathway. However, expressions of bone-related genes and MMPs were regulated by SLIM-independent pathway. Our present results suggest that the aberrant accumulation of STAT1 protein induced by loss of PKR regulate osteoblast differentiation through both SLIM/STAT1-dependent and -independent pathways.

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  • Calcineurin regulates phosphorylation status of transcription factor osterix Reviewed

    Hirohiko Okamura, Bruna Rabelo Amorim, Jie Wang, Kaya Yoshida, Tatsuji Haneji

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   379 ( 2 )   440 - 444   2009.2

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  • Calcineurin regulates phosphorylation satus of transcriptionfactor osterix Reviewed

    Hirohiko Okamura, Bruna Rabelo Amorim, Jie Wang, Kaya Yoshida, Tatsuji Haneji

    Biochemical and Biophysical Research Communications   Vol.379 ( No.2 )   440 - 444   2009

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    Osterix is an osteoblast-specific transcriptional factor that is essential for osteoblast differentiation and bone formation. Calcineurin regulates bone formation through modulating osteoblast differentiation. However, post-translational modification of osterix such as phosphorylation and interactions between osterix and calcineurin remains unclear. In the present study, we demonstrated that calcineurin interacted with osterix determined by immunoprecipitation assay and Western analysis. Immunocytochemical study also revealed that osterix and calcineurin were co-localized in nucleus. Deletion of calcineurin binding motif on osterix molecule disrupted osterix-calcineurin interaction. Phosphorylation status of osterix was augmented by treatment with phosphatase inhibitors, FK506 and calyculin A. In contrast, treatment of recombinant calcineurin reduced phosphorylation status of osterix. Our present study suggests that calcineurin has an important role in the function of osterix through its modification of phosphorylation.

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  • Histone H1.2 is translocated to mitochondria and associates with Bak in bleomycin-induced apoptotic cells Reviewed

    Hirohiko Okamura, Kaya Yoshida, Bruna Rabelo Amorim, Tatsuji Haneji

    Journal of Cellular Biochemistry   Vol.103 ( No.5 )   1488 - 1496   2008.4

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    Bleomycin induces single- and double-stranded breaks in DNA, with consequent mitochondrial membrane aberrations that lead to the apoptotic cell death. It is poorly understood how DNA damage-inducing apoptotic signals are transmitted to mitochondria, from which apoptotic factors are released into the cytoplasm. Here, we investigated the localization of histone H1.2 in the bleomycin-treated human squamous carcinoma SCCTF cells. The presence of DNA double-strand breaks in the bleomycin-treated cells was examined by Western analysis using antibody against phosphorylated histone H2AX (gamma-H2AX). Incubation of SCCTF cells for 48 h with 10 microM bleomycin induced apoptosis, as determined by cleavage of lamin B1 to 28 kDa fragment and DNA ladder formation. The mitochondrial permeabilization causing apoptotic feature was also detected with MitoCapture in the bleomycin-treated cells. Histone H1.2 was translocated from the nucleus to the mitochondria after treatment with bleomycin and co-localized with Bak in mitochondria. Our present results suggest that histone H1.2 plays an important role in transmitting apoptotic signals from the nucleus to the mitochondria following double-stranded breaks of DNA by bleomycin.

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  • Histone H1.2 is translocated to mitochondria and associates with Bak in bleomycin-induced apoptotic cells Reviewed

    Hirohiko Okamura, Kaya Yoshida, Bruna Rabelo Amorim, Tatsuji Haneji

    JOURNAL OF CELLULAR BIOCHEMISTRY   103 ( 5 )   1488 - 1496   2008.4

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  • The transcriptional factor Osterix directly interacts with RNA helicase A. Invited Reviewed

    Amorim BR, Okamura H, Yoshida K, Wang J, Qiu LH, Haneji T

    Ocean Papers & Printers, New Delhi   216 - 222   2008

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  • Cobalt chloride induces apoptosis and zinc chloride suppresses cobalt-induced apoptosis by Bcl-2 expression in human submandibular gland HSG cells Reviewed

    Kazumi Akita, Hirohiko Okamura, Kaya Yoshida, Hiroyuki Morimoto, Hiroaki Ogawa-Iyehara, Tatsuji Haneji

    INTERNATIONAL JOURNAL OF ONCOLOGY   31 ( 4 )   923 - 929   2007.10

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  • Calyculin A induces apoptosis and stimulates phosphorylation of p65NF-kappa B in human osteoblastic osteosarcoma MG63 cells Reviewed

    Hiroaki Tanaka, Kaya Yoshida, Hirohiko Okamura, Hiroyuki Morimoto, Toshihiko Nagata, Tatsuji Haneji

    INTERNATIONAL JOURNAL OF ONCOLOGY   31 ( 2 )   389 - 396   2007.8

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  • Differential expression of protein phosphatase type 1 isotypes and nucleolin during cell cycle arrest Reviewed

    Hiroyuki Morimoto, Akiko Ozaki, Hirohiko Okamura, Kaya Yoshida, Bruna Rabelo Amorim, Hiroaki Tanaka, Seiichiro Kitamura, Tatsuji Haneji

    CELL BIOCHEMISTRY AND FUNCTION   25 ( 4 )   369 - 375   2007.7

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  • Calyculin A stimulates the expression of TNF-alpha mRNA via phosphorylation of Akt in mouse osteoblastic MC3T3-E1 cells Reviewed

    Lihong Qiu, Kaya Yoshida, Bruna Rabelo Amorim, Hirohiko Okamura, Tatsuji Haneji

    MOLECULAR AND CELLULAR ENDOCRINOLOGY   271 ( 1-2 )   38 - 44   2007.6

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  • The transcriptional factor Osterix directly interacts with RNA helicase A Reviewed

    Bruna Rabelo Amorim, Hirohiko Okamura, Kaya Yoshida, Lihong Qiu, Hiroyuki Morimoto, Tatsuji Haneji

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   355 ( 2 )   347 - 351   2007.4

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  • Expression of PTEN and Akt phosphorylation in lipopolysaccharide-treated NIH3T3 cells Reviewed

    Hirohiko Okamura, Kaya Yoshida, Eiko Sasaki, Lihong Qiu, Bruna Rabelo Amorim, Hiroyuki Morimoto, Tatsuji Haneji

    CELL BIOLOGY INTERNATIONAL   31 ( 2 )   119 - 125   2007.2

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    DOI： 10.1016/j.cellbi.2006.09.014

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  • Role of transcription factors in multidrug resistance and apoptosis. Invited Reviewed

    Okamura H, Haneji T

    Dentistry in Japan   43 ( 1 )   1 - 6   2007

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  • 口腔扁平上皮癌細胞の薬剤耐性とアポトーシス ~ 転写調節因子の役割 ~ Reviewed

    岡村 裕彦

    四国歯学会雑誌   19   171 - 17   2007

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  • Okadaic acid induces phosphorylation of p65NF-kappa B on serine 536 and activates NF-kappa B transcriptional activity in human osteoblastic MG63 tells Reviewed

    Akiko Ozaki, Hiroyuki Morimoto, Hiroaki Tanaka, Hirohiko Okamura, Kaya Yoshida, Bruna Rabelo Amorim, Tatsuji Haneji

    JOURNAL OF CELLULAR BIOCHEMISTRY   99 ( 5 )   1275 - 1284   2006.12

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    DOI： 10.1002/jcb.20873

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  • Double-stranded RNA-dependent protein kinase is required for bone calcification in MC3T3-E1 cells in vitro Reviewed

    K Yoshida, H Okamura, BR Amorim, A Ozaki, H Tanaka, H Morimoto, T Haneji

    EXPERIMENTAL CELL RESEARCH   311 ( 1 )   117 - 125   2005.11

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    DOI： 10.1016/j.yexcr.2005.09.006

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  • Okadaic acid induces tyrosine phosphorylation of I kappa B alpha that mediated by PKR pathway in human osteoblastic MG63 cells Reviewed

    H Morimoto, A Ozaki, H Okamura, K Yoshida, S Kitamura, T Haneji

    MOLECULAR AND CELLULAR BIOCHEMISTRY   276 ( 1-2 )   211 - 217   2005.8

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    DOI： 10.1007/s11010-005-4440-y

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  • PTEN expression elicited by EGR-1 transcription factor in calyculin a-induced apoptotic cells Reviewed

    H Okamura, K Yoshida, H Morimoto, T Haneji

    JOURNAL OF CELLULAR BIOCHEMISTRY   94 ( 1 )   117 - 125   2005.1

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    DOI： 10.1002/jcb.20283

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  • Okadaic acid induces apoptosis through double-stranded RNA-dependent protein kinase/eukaryotic initiation factor-2 alpha pathway in human osteoblastic MG63 cells Reviewed

    H Morimoto, H Okamura, K Yoshida, S Kitamura, T Haneji

    JOURNAL OF BIOCHEMISTRY   136 ( 4 )   433 - 438   2004.10

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    DOI： 10.1093/jb/mvh144

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  • Transcription factor NF-Y regulates mdr1 expression through binding to inverted CCAAT sequence in drug-resistant human squamous carcinoma cells Reviewed

    H Okamura, K Yoshida, E Sasaki, H Morimoto, T Haneji

    INTERNATIONAL JOURNAL OF ONCOLOGY   25 ( 4 )   1031 - 1037   2004.10

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  • Double-stranded RNA mediates selective gene silencing of protein phosphatase type 1 delta isoform in HEK-293 cells Reviewed

    H Morimoto, H Okamura, K Yoshida, S Kitamura, T Hanejl

    JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY   19 ( 4 )   327 - 331   2004.8

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    DOI： 10.1080/14756360410001704452

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  • Okadaic acid stimulates expression of Fas receptor and Fas ligand by activation of nuclear factor kappa-B in human oral squamous carcinoma cells Reviewed

    M Fujita, K Goto, K Yoshida, H Okamura, H Morimoto, S Kito, J Fukuda, T Haneji

    ORAL ONCOLOGY   40 ( 2 )   199 - 206   2004.2

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    DOI： 10.1016/S1368-8375(03)00152-0

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  • 薬剤耐性扁平上皮癌細胞におけるアポトーシスと転写調節因子 Reviewed

    岡村 裕彦

    徳島大学大学院歯学研究科   17 ( 1 )   123 - 136   2004

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  • Transblot and cytochemical identification of avidin-interacting proteins in mitochondria of cultured cells Reviewed

    E Sasaki, Y Okamoto, K Yoshida, H Okamura, K Shimizu, F Nasu, H Morimoto, T Haneji

    HISTOCHEMISTRY AND CELL BIOLOGY   120 ( 4 )   327 - 333   2003.10

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    DOI： 10.1007/s00418-003-0572-x

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  • Cleavage of nucleolin and argyrophilic nucleolar organizer region associated proteins in apoptosis-induced cells Reviewed

    S Kito, K Shimizu, H Okamura, K Yoshida, H Morimoto, M Fujita, Y Morimoto, T Ohba, T Haneji

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   300 ( 4 )   950 - 956   2003.1

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    DOI： 10.1016/S0006-291X(02)02942-X

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  • Okadaic acid stimulates the receptor activator of nuclear factor-kappa B ligand (RANKL) in mouse osteoblastic cells. Reviewed

    Yoshida K, Okamura H, Morimoto H, Nagata T, Haneji T

    Biomed. Res.   14 ( 2 )   126 - 132   2003

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  • Suppression of Egr-1 expression in human oral squamous carcinoma cells by okadaic acid Reviewed

    H Okamura, H Morimoto, M Fujita, F Nasu, E Sasaki, T Haneji

    ORAL ONCOLOGY   38 ( 8 )   779 - 784   2002.12

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    DOI： 10.1016/S1368-8375(02)00039-8

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  • Suppression of Egr-1 expression in human oral squamous carcinoma cells by okadaic acid Reviewed

    H. Okamura, H. Morimoto, M. Fujita, F. Nasu, E. Sasaki, T. Haneji

    Oral Oncology   38 ( 8 )   779 - 784   2002.12

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    DOI： 10.1016/S1368-8375(02)00039-8

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  • Interaction of protein phosphatase 1 delta with nucleolin in human osteoblastic cells Reviewed

    H Morimoto, H Okamura, T Haneji

    JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY   50 ( 9 )   1187 - 1193   2002.9

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    DOI： 10.1177/002215540205000905

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  • Peplomycin-induced apoptosis in oral squamous carcinoma cells depends on bleomycin sensitivity Reviewed

    H Okamura, H Morimoto, T Haneji

    ORAL ONCOLOGY   37 ( 4 )   379 - 385   2001.6

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    DOI： 10.1016/S1368-8375(00)00101-9

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  • Alteration of argyrophilic nucleolar organizer region associated (Ag-NOR) proteins in apoptosis-induced human salivary gland cells and human oral squamous carcinoma cells Reviewed

    Y Morimoto, S Kito, T Ohba, H Morimoto, H Okamura, T Haneji

    JOURNAL OF ORAL PATHOLOGY & MEDICINE   30 ( 4 )   193 - 199   2001.4

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    DOI： 10.1034/j.1600-0714.2001.300401.x

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  • Upregulation of the expression of Fas antigen and Fas ligand in a human submandibular gland ductal cell line by okadaic acid Reviewed

    Y Morimoto, H Morimoto, H Okamura, K Nomiyama, N Nakamuta, S Kobayashi, S Kito, T Ohba, T Haneji

    ARCHIVES OF ORAL BIOLOGY   45 ( 8 )   657 - 666   2000.8

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    DOI： 10.1016/S0003-9969(00)00038-8

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MISC

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Presentations

  • Detection of extracellular Z-form DNA in mature Porphyromonas gingivalis biofilm

    Zheng Yilin, Sitosari Heriati, Weng Yao, 味野範子, 福原瑶子, 池亀美華, 岡村裕彦

    日本解剖学会第76回中国・四国支部学術集会 

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    Event date： 2022.10.29 - 2022.10.30

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  • Inhibition of protein phosphatase 2 by okadaic acid changes nucleocytoplasmic O-GlcNAc transferase localization

    Sitosari Heriati, Weng Yao, Zheng Yilin, 福原瑶子, 池亀美華, 岡村裕彦

    日本解剖学会第76回中国・四国支部学術集会 

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    Event date： 2022.10.29 - 2022.10.30

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  • Porphyromonas gingivalis菌によるバイオフィルム形成の至適条件の確立

    Zheng Yilin, Sitosari Heriati, Weng Yao, 塩津範子, 福原瑶子, 池亀美華, 岡村裕彦

    第39回分子病理学研究会 

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    Event date： 2022.7.8 - 2022.7.9

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  • 間欠的・持続的伸展刺激受容後における骨芽細胞の経時的変化

    竹本史子, 福原瑶子, 池亀美華, 上岡寛, 岡村裕彦

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    Event date： 2022.3.27 - 2022.3.29

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  • オホーツク文化人の歯石を対象とした古代プロテオミクス解析の検討

    竹本史子, 福原瑶子, 池亀美華, 上岡寛, 岡村裕彦

    第127回日本解剖学会総会・全国学術集会 

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    Event date： 2022.3.27 - 2022.3.29

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  • O-GlcNAcylation drives calcium signaling towards osteoblast differentiation

    Weng Yao, Heriati Sitosari, 福原瑶子, 池亀美華, 岡村裕彦

    日本解剖学会第75回中国・四国支部学術集会 

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    Event date： 2021.10.30

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  • O-GlcNAcylation affects the growth and migration ability of human oral squamous carcinoma cells

    Heriati Sitosari, Weng Yao, 福原瑶子, 池亀美華, 岡村裕彦

    日本解剖学会第75回中国・四国支部学術集会 

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    Event date： 2021.10.30

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  • 歯周病原菌に感染したマクロファージ由来の細胞外小胞は胎盤の血管形成を阻害する

    棚井あいり，福原瑶子，江口傑徳，植田幸嗣，吉田賀弥，岡村裕彦

    第8回日本細胞外小胞学会  2021.10.18  日本細胞外小胞学会

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    Event date： 2021.10.18 - 2021.10.19

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：京都大学（オンライン）   Country：Japan  

  • 歯周病原菌に感染したマクロファージ由来の細胞外小胞は胎盤の血管形成を阻害する

    棚井あいり, 福原瑶子, 江口傑徳, 植田幸嗣, 吉田賀弥, 岡村裕彦

    第29回硬組織再生生物学会学術大会 

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    Event date： 2021.10.18 - 2021.10.19

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  • 第29回硬組織再生生物学会学術大会

    岡村裕彦

    第29回硬組織再生生物学会学術大会 

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    Event date： 2021.8.28

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  • In Vitroで骨芽細胞分化を促進する一軸的伸展刺激条件の検討

    竹本史子, 福原瑶子, 池亀美華, 上岡寛, 岡村裕彦

    第29回硬組織再生生物学会学術大会 

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    Event date： 2021.8.28

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  • The role of O-GlcNAc transferase in osteoblast differentiation

    Yao Weng, Airi Tanai, Yoko Fukuhara, Mika Ikegame, Hirohiko Okamura

    第126回日本解剖学会総会・全国学術集会，第98回日本生理学学会大会 

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    Event date： 2021.3.28 - 2021.3.30

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  • 母体腸内細菌叢の有無が胎児骨格形成に与える影響 Invited

    福原瑶子, 服部高子, 池亀美華, 久保田聡, 岡村裕彦

    第62回歯科基礎医学会学術大会 

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    Event date： 2020.9.11 - 2020.10.19

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  • Effects of maternal gut microbiome on fetal endochondral bone formation Invited

    Uchida-Fukuhara Y, Hattori T, Ikegame M, Kubota S, Okamura H

    第62回歯科基礎医学会アップデートシンポジウム05 発生と疾患にみる新たな細胞間コミュニケーション 

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    Event date： 2020.9.11 - 2020.10.19

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  • 歯周病原菌-マクロファージ間コミュニケーションに起因する全身疾患発症機構 Invited

    吉田賀弥, 岡村裕彦

    第62回歯科基礎医学会学術大会 

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    Event date： 2020.9.11 - 2020.10.19

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  • 肺および口腔上皮細胞におけるPorphyromonas gingivalis由来の細胞外小胞の障害性

    山口真輝, 塩津範子, 竹本史子, 池亀美華, 吉田賀弥, 上岡寛, 鳥井康弘, 佐々木朗, 岡村裕彦

    第62回歯科基礎医学会 

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    Event date： 2020.9.11 - 2020.10.19

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  • 骨芽細胞における転写共役因子Vgll3の役割

    池亀美華，岡村裕彦

    第125回日本解剖学会総会・全国学術集会  2020.3.25 

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    Event date： 2020.3.25 - 2020.3.27

    Language：Japanese   Presentation type：Oral presentation (general)  

  • 骨芽細胞における転写共役因子Vgll3の役割

    池亀美華, 岡村裕彦

    第125回日本解剖学会総会・全国学術集会, 2020年3月25-27日, ANAクラウンプラザホテル宇部 

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    Event date： 2020.3.25 - 2020.3.26

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  • クォーラムセンシング因子は骨芽細胞の分化および細胞死に関与する International coauthorship

    岡村裕彦，Guo Jiajie，Weng Yao，Yuan Haoze，吉田賀弥，池亀美華

    日本解剖学会第74回中国・四国支部学術集会  2019.10.26 

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    Event date： 2019.10.26 - 2019.10.27

    Language：Japanese   Presentation type：Oral presentation (general)  

  • The expression and role of O-GlcNAc transferase on osteoblast and osteoclast differentiation International coauthorship

    2019.10.26 

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    Event date： 2019.10.26 - 2019.10.27

    Language：English   Presentation type：Oral presentation (general)  

  • The role of Vgll3 co-transcription factor during osteoblast differentiation International coauthorship

    Yuan Haoze, Mika Ikegame, Weng Yao, Guo Jiajie, Hirohiko Okamura

    2019.10.26 

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    Event date： 2019.10.26 - 2019.10.27

    Language：English   Presentation type：Oral presentation (general)  

  • The expression and role of O-GlcNAc transferase on osteoblast and osteoclast differentiation

    Weng Yao, Guo Jiajie, Yuan Haoze, 吉田賀弥, 池亀美華, 岡村裕彦

    日本解剖学会第74回中国・四国支部学術集会 

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    Event date： 2019.10.26 - 2019.10.27

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  • The role of Vgll3 co-transcription factor during osteoblast differentiation

    Yuan Haoze, Mika Ikegame, Weng Yao, Guo Jiajie, Hirohiko Okamura

    日本解剖学会第74回中国・四国支部学術集会 

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    Event date： 2019.10.26 - 2019.10.27

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  • Porphyromonas gingivalis感染マクロファージの細胞外小胞が多臓器に及ぼす影響

    吉田賀弥，吉田佳世，尾崎和美，岡村裕彦

    第6回日本細胞外小胞学会  2019.10.24 

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    Event date： 2019.10.24 - 2019.10.25

    Language：Japanese   Presentation type：Oral presentation (general)  

  • Porphyromonas gingivalis感染マクロファージの細胞外小胞が多臓器に及ぼす影響

    吉田賀弥, 吉田佳世, 尾崎和美, 岡村裕彦

    第6回日本細胞外小胞学会 

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    Event date： 2019.10.24 - 2019.10.25

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  • 骨芽細胞におけるVgll3の発現

    池亀美華，内部健太，岡村裕彦

    第61回歯科基礎医学会学術大会  2019.10.12 

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    Event date： 2019.10.12 - 2019.10.14

    Language：Japanese   Presentation type：Oral presentation (general)  

  • 骨芽細胞の分化と細胞死におけるクォーラムセンシング因子AHLの影響

    岡村裕彦，池亀美華，吉田賀弥

    第61回歯科基礎医学会学術大会  2019.10.12 

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    Event date： 2019.10.12 - 2019.10.14

    Language：Japanese   Presentation type：Oral presentation (general)  

  • 骨芽細胞におけるVgll3の発現

    池亀美華, 内部健太, 岡村裕彦

    第61回歯科基礎医学会学術大会 

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    Event date： 2019.10.12 - 2019.10.14

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  • 骨芽細胞の分化と細胞死におけるクォーラムセンシング因子AHLの影響

    岡村裕彦, 池亀美華, 吉田賀弥

    第61回歯科基礎医学会学術大会 

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    Event date： 2019.10.12 - 2019.10.14

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  • 軟骨形成におけるレチノイン酸シグナルの役割 Invited

    内部健太, 池亀美華, 岩本容泰, 岡村裕彦

    第60回日本組織細胞化学会総会・学術集会 

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    Event date： 2019.9.19 - 2019.9.21

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  • Effect of bacterial quorum sensing factor on osteoblast differentiation and apoptosis Invited

    Hirohiko Okamura, Jiajie Guo

    The 2nd International Conference on Bioinformatics, Biotechnology, and Biomedical Engineering 

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    Event date： 2019.9.12 - 2019.9.13

    Language：English  

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  • The effects of outer membrane vesicles derived from Porphyromonas gingivalis on hepatic glucose metabolisms.

    Kaya Yoshida, Hirohiko Okamura

    Annual meeting 2019 International Society for Extracellular vesicles 

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    Event date： 2019.4.24 - 2019.4.28

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  • 卵巣摘出ラットの骨粗鬆化における副甲状腺ホルモンとメラトニンの併用効果

    池亀美華，田中みか子，江尻貞一，服部淳彦，高尾亮子，内部健太，岡村裕彦

    第124回日本解剖学会総会・全国学術集会  2019.3.27 

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    Event date： 2019.3.27 - 2019.3.29

    Language：Japanese   Presentation type：Oral presentation (general)  

  • 歯周病原菌が感染したマクロファージが放出するエクソソームには病原因子やヒストン蛋白が含まれる

    岡村裕彦，内部健太，池亀美華，吉田賀弥

    第124回日本解剖学会総会・全国学術集会  2019.3.27 

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    Event date： 2019.3.27 - 2019.3.29

    Language：Japanese   Presentation type：Oral presentation (general)  

  • 歯周病原菌が感染したマクロファージが放出するエクソソームには病原因子やヒストン蛋白が含まれる

    岡村裕彦, 内部健太, 池亀美華, 吉田賀弥

    第124回日本解剖学会総会・全国学術集会 

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  • 高グルコース濃度下の骨芽細胞分化における蛋白質脱リン酸化酵素の活性とO-GlcNAc転移酵素の局在

    岡村裕彦, Heriati Sitosari, 福原瑶子, 池亀美華

    第17回日本臨床ストレス応答学会大会  2023.11.18 

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  • 骨芽細胞の分化における蛋白質脱リン酸化酵素の活性とO-GlcNAc転移酵素の局在

    岡村裕彦, Heriati Sitosari, 福原瑶子, 池亀美華

    第77回日本解剖学会中国・四国支部学術集会  2023.10.15 

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  • 口腔と全身性疾患を繋ぐ細胞外小胞の動態 Invited

    岡村裕彦

    第4回「医学と数理」研究会  2023.9.30 

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  • 骨芽細胞の分化における蛋白質脱リン酸化酵素の活性とO-GlcNAc転移酵素の局在

    Heriati Sitosari, 福原瑶子, 池亀美華, 岡村裕彦

    第65回歯科基礎医学会学術大会  2023.9 

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  • The interaction of O-GlcNAc transferase and protein phosphatase 2A: crosstalk study of phosphorylation and O-GlcNAcylation

    Heriati Sitosari, Ikkei Morimoto, Yao Weng, Yilin Zheng, Yoko Fukuhara, Mika Ikegame, Hirohiko Okamura

    2023.3 

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  • 液-液相分離は-カテニンの細胞内局在を制御する

    加藤愛里, 福原瑶子, Heriati Sitosari, 池亀美華, 岡村裕彦

    第128回日本解剖学会総会学術集会  2023.3 

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  • O-GlcNAcylation affects the growth and migration ability of human oral squamous carcinoma cells International coauthorship

    2021.10.30 

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    Country：Japan  

  • O-GlcNAcylation drives calcium signaling towards osteoblast differentiation International coauthorship

    2021.10.30 

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    Country：Japan  

  • Porphyromonas gingivalisはマクロファージの細胞外小胞を介して胎児の成長を遅延した

    棚井あいり，福原瑶子，河合穂高，江口傑徳，池亀美華，吉田賀弥，岡村裕彦

    第29回硬組織再生生物学会学術大会  2021.8.28 

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  • 骨関連細胞における蛋白質脱リン酸化酵素と糖鎖修飾の役割 Invited

    岡村裕彦

    第29回硬組織再生生物学会学術大会  2021.8.28 

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  • In Vitroで骨芽細胞分化を促進する一軸的伸展刺激条件の検討

    竹本史子，福原瑶子，池亀美華，上岡寛，岡村裕彦

    第29回硬組織再生生物学会学術大会  2021.8.28 

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  • 歯周病原菌由来の細胞外小胞は胎盤の形成および胎児の成長を阻害する

    棚井あいり（指導：岡村裕彦）

    第126回日本解剖学会総会・全国学術集会，第98回日本生理学学会大会  2021.3.28 

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  • The role of O-GlcNAc transferase in osteoblast differentiation International coauthorship

    Yao Weng, Airi Tanai, Yoko Fukuhara, Mika Ikegame, Hirohiko Okamura.

    2021.3.28 

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  • The effect ofPorphyromonas gingivalis outer membrane vesicles on lung and oral epithelial cells

    2020.9.11 

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  • Effects of maternal gut microbiome on fetal endochondral bone formation. Invited

    2020.9.11 

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  • PP2A is involved in chondrogenic differentiation

    Weng Yao, Guo Jiajie, 吉田賀弥, 内部健太, 池亀美華, 岡村裕彦

    日本解剖学会第73回中国・四国支部学術集会  2018.10.20 

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  • キンギョのウロコにおけるスクレロスチンの発現局在

    池亀美華, 北村敬一郎, 服部淳彦, 鈴木信雄, 内部健太, 岡村裕彦

    日本解剖学会第73回中国・四国支部学術集会  2018.10.20 

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  • 骨格形成におけるレチノイン酸レセプターシグナルの機能の検討

    住谷友祐, 内部健太, 池亀美華, 上岡寛, 岡村裕彦

    日本解剖学会第73回中国・四国支部学術集会  2018.10.20 

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  • マクロファージ由来のエクソソームによって運ばれる歯周病原因子の動態

    岡村裕彦, Guo Jiajie, Weng Yao, 内部健太, 池亀美華, 吉田賀弥

    日本解剖学会第73回中国・四国支部学術集会  2018.10.20 

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  • Effect of N-Acyl Homoserine Lactone (AHL) on differentiation and apoptosis in osteoblastic MC3T3 cells.

    2018.10.20 

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  • 骨粗鬆症モデルラットにおける副甲状腺ホルモンとメラトニンの併用効果

    池亀美華, 田中みか子, 江尻貞一, 服部淳彦, 高尾亮子, 内部健太, 岡村裕彦

    第60回歯科基礎医学会学術大会  2018.9.5 

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  • Porphyromonas gingivalis感染したマクロファージが産生する膜小胞が肝臓糖代謝に及ぼす影響

    吉田賀弥, 藤原奈津美, 尾崎和美, 内部健太, 池亀美華, 岡村裕彦

    第60回歯科基礎医学会学術大会  2018.9.5 

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  • Extracellular vesicles from Porphyromonas gingivalis-infected macrophages include histone protein and translocate to the liver. International conference

    10th annual meeting of Japanese association for RNAi・5th annual meeting of Japanese Society of extracellular vesicles  2018.8.29 

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  • マクロファージ由来のエクソソームによって運ばれる歯周病原菌因子の動態

    岡村裕彦, 内部健太, 池亀美華, 吉田賀弥

    第37回分子病理研究会 はがくれシンポジウム  2018.7.7 

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  • ヒストン脱メチル化酵素Jmjd3は転写調節因子Runx2とOsterixを介して骨芽細胞分化を制御する

    木目龍大, 内部健太, 池亀美華, 吉田賀弥, 岡村裕彦

    第123回日本解剖学会総会・全国学術集会  2018.3.28 

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  • 機械的伸展刺激によるCCN1/CYR61発現促進へのYAP/TAZ核移行シグナルの関与

    池亀美華, 岡村裕彦, 内部健太

    日本解剖学会第72回中国・四国支部学術集会  2017.10.28 

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  • ヒストン脱メチル化酵素Jmjd3による骨芽細胞のアポトーシス制御機構

    木目龍大, 内部健太, 池亀美華, 岡村裕彦

    日本解剖学会第72回中国・四国支部学術集会  2017.10.28 

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  • 研究活動の楽しさと出会い

    岡村 裕彦

    2017.10.1 

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  • Enjoy Research! International conference

    OKAMURA Hirohiko

    2017.9.25 

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  • RARγシグナリングは成長板軟骨細胞分化・成熟を制御する

    内部健太, 池亀美華, 岡村裕彦

    第59回歯科基礎医学会学術大会  2017.9.16 

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  • 骨芽細胞の分化におけるプロテインホスファターゼPP2A Cαの役割とその標的因子

    岡村裕彦, 吉田賀弥, 内部健太, 池亀美華

    第59回歯科基礎医学会学術大会  2017.9.16 

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  • 伸展刺激による骨芽細胞増殖促進に関与する新規遺伝子の解明

    池亀美華, 内部健太, 岡村裕彦

    第59回歯科基礎医学会学術大会  2017.9.16 

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  • プロテインホスファターゼPP2Aは骨肉腫細胞の増殖・転移能を制御する

    岡村裕彦, 森本景之, 羽地達次, 池亀美華, 内部健太

    第36回分子病理研究会  2017.7.21 

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  • 骨髄腫腫瘍進展と骨破壊病変形成におけるTAK-1の枢軸的役割

    寺町順平, 日浅雅博, 天真寛文, 岡村裕彦, 安倍正博, 羽地達次

    第122回日本解剖学会総会・全国学術集会  2017.3.28 

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  • ヒストン脱メチル化酵素Jmjd3はBcl-2およびPKD1の発現を介して骨芽細胞のアポトーシスを制御する

    岡村裕彦, Yang Di, 寺町順平

    第122回日本解剖学会総会・全国学術集会  2017.3.28 

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  • 骨髄腫の腫瘍進展と骨破壊病変形成におけるTAK1の枢軸的な役割

    寺町順平, 日浅雅博, 岡村裕彦, 安倍正博, 羽地達次

    日本解剖学会第71回中国・四国支部学術集会  2016.10.22 

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  • 骨芽細胞の分化と機能におけるプロテインホスファターゼPP2A Cαの役割

    岡村裕彦, 寺町順平

    日本解剖学会第71回中国・四国支部学術集会  2016.10.22 

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  • TAK-1阻害による腫瘍進展の抑制と骨病変の改善効果

    寺町順平, 岡村裕彦, 羽地達次

    第58回歯科基礎医学会学術大会  2016.8.24 

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  • 骨芽細胞と脂肪細胞の分化におけるプロテインホスファターゼPP2A Cαの役割

    岡村裕彦, 吉田賀弥, 寺町順平

    第58回歯科基礎医学会学術大会  2016.8.24 

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  • PKRは骨芽細胞においてPorphylomonas gingivalisが誘導するNLRP3発現をNF-B経路を介して制御する

    吉田賀弥, 岡村裕彦

    第58回歯科基礎医学会学術大会  2016.8.24 

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  • PP2A CαはWnt/β-catenin経路とPPARgammaの発現を介して脂肪細胞の分化を調節する

    岡村裕彦, 羽地達次

    第121回日本解剖学会総会・全国学術集会  2016.3.28 

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  • 炎症性骨破壊におけるPKRの枢軸的役割

    寺町順平, 篠原宏貴, 稲垣裕司, 岡村裕彦, 永田俊彦, 羽地達次

    第135回徳島生物学会  2015.12.23 

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  • 骨形成および骨芽細胞の分化に関する研究とその手法

    岡村裕彦, 楊諦, 寺町順平, 羽地達次

    第135回徳島生物学会  2015.12.23 

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  • Pim-2を標的とした骨髄腫細胞における骨破壊の抑制

    寺町順平, 日浅雅博, 岡村裕彦, 安部正博, 羽地達次

    日本解剖学会第70回中国・四国支部学術集会  2015.10.24 

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  • 骨芽細胞と脂肪細胞の分化におけるプロテインホスファターゼPP2A Cαの役割

    岡村裕彦, 寺町順平, 羽地達次

    日本解剖学会第70回中国・四国支部学術集会  2015.10.24 

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  • ラット臼歯部咬合支持の喪失がオトガイ舌骨筋および咬筋の筋組成へ与える影響

    馬場拓朗, 岡村裕彦, Yang Di, 永尾寛, 羽地達次, 市川哲雄

    日本解剖学会第70回中国・四国支部学術集会  2015.10.24 

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  • PKRやインフラマソームがP. gingivalisを感染させた骨芽細胞において骨吸収に関連する因子の発現に与える影響

    吉田賀弥, 岡村裕彦, 尾崎和美

    第57回歯科基礎医学会学術大会・総会  2015.9.11 

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  • プロテインホスファターゼPP2A Cαは、骨芽細胞と脂肪細胞の分化を制御する

    岡村裕彦, 寺町順平, 羽地達次

    第57回歯科基礎医学会学術大会・総会  2015.9.11 

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  • Pim阻害による骨髄腫骨吸収亢進の抑制

    寺町順平, 岡村裕彦, 羽地達次

    第57回歯科基礎医学会学術大会・総会  2015.9.11 

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  • Cleavage of nucleolin and argyrophilic nuclear organizer region associated proteins in apoptosis-induced cells International conference

    Haneji T, Yoshida K, Okamura H, Qiu LH

    The 7th Chinese Congress on Oral Pathology  2006.10 

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  • 蛋白質脱リン酸化酵素と核内リン酸化蛋白の細胞内局在変化

    森本景之, 岡村裕彦, 羽地達次

    第106回日本解剖学会総会 ミニシンポジウム  2001.4.2 

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Awards

  • Educational Distinguished Service Award in Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

    2023.1   Okayama University  

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  • 高田充基礎医学賞

    2005  

    岡村 裕彦

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  • 康楽賞

    2004   財団法人康楽會  

    岡村 裕彦

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Research Projects

  • 口腔癌の発症・進展における歯周病原菌由来細胞外膜小胞の関わり

    Grant number：24K13115  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    中谷 貴恵, 山本 哲也, 岡村 裕彦, 笹部 衣里

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    Grant amount：\4550000 （ Direct expense: \3500000 、 Indirect expense：\1050000 ）

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  • Analysis of extracellular vesicles esponsible for transplacental transduction between mother and child

    Grant number：23K18431  2023.06 - 2025.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

    岡村 裕彦, 河合 穂高, 福原 瑶子

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    Grant amount：\6500000 （ Direct expense: \5000000 、 Indirect expense：\1500000 ）

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  • 癌骨破壊病変において新規破骨細胞形成促進因子Angiogeninが果たす役割の解明

    Grant number：23H03100  2023.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(B)

    伊原木 聰一郎, 長塚 仁, 中野 敬介, 岡村 裕彦

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    Grant amount：\18720000 （ Direct expense: \14400000 、 Indirect expense：\4320000 ）

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  • 癌骨破壊病変において新規破骨細胞形成促進因子Angiogeninが果たす役割の解明

    Grant number：23K27790  2023.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(B)

    伊原木 聰一郎, 長塚 仁, 岡村 裕彦, 中野 敬介

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    Grant amount：\18720000 （ Direct expense: \14400000 、 Indirect expense：\4320000 ）

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  • 歯周病由来「細胞外小胞」に着目した一生涯トータルヘルスケアの検討

    Grant number：23K09458  2023.04 - 2026.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    福原 瑶子, 岡村 裕彦, 池亀 美華, 江國 大輔

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    Grant amount：\4810000 （ Direct expense: \3700000 、 Indirect expense：\1110000 ）

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  • Alteration of extracellular DNA structure during maturation of oral biofilm

    Grant number：23K09504  2023.04 - 2026.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    味野 範子, 岡村 裕彦, 福原 瑶子

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    Grant amount：\4680000 （ Direct expense: \3600000 、 Indirect expense：\1080000 ）

    歯周病は，口腔微生物が形成するバイオフィルムである歯垢が歯肉溝に沈着することにより進行する。バイオフィルムの形成は細胞外DNAを含む細胞外基質（マトリクス）の集積により生じる。バイオフィルムの成熟に伴いマトリクスの結合の強まりが，その構造を強固にし，歯垢除去を困難にする。そのため，歯周病の予防には，マトリクスの結合を抑制し，バイオフィルムの成熟を妨げる薬剤の開発が期待される。我々は，歯周病原菌のバイオフィルム成熟過程においてマトリクスにおける細胞外DNAに構造変化が生じることを見出した。この細胞外DNAの構造変化は酵素による分解や免疫を抑制することでバイオフィルムをより強固にし，歯周病の進行に関与すると考えられる。
    本研究は，歯周病原菌のバイオフィルム成熟過程において細胞外DNAの構造変化がどのような役割をもつか解明することを目的とした。
    高分子複合体であるバイオフィルムでは，細胞外DNAは構造を支える『梁』の役割を担っている。細胞外DNA には右巻きと左巻きの異なる二重らせん構造を示すものが存在する。B型DNA（B-DNA）は，一般的な右巻きの構造を示し，DNA分解酵素に感受性が高い。Z型DNA（Z-DNA）は，非一般的で左巻きの構造を示し， DNA分解酵素に抵抗性を示す。しかし，歯周病原菌のバイオフィルムにおける細胞外DNAの構造変化は明らかでなかった。
    P. gingivalis を培養し，バイオフィルムを形成させた。B-DNAおよびZ-DNAに対する抗体を用いた免疫染色を行う。その結果，P. gingivalis のバイオフィルム成熟過程でZ-DNAの存在量が増加することが分かった。

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  • 口腔癌の発症と進行における歯周病原菌由来の小胞の役割

    Grant number：KKCS20220523004  2022.09 - 2023.03

    協和発酵キリン 

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    Authorship：Principal investigator 

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  • 細胞外DNAに着目した新規歯周病治療開発のための基礎的研究

    Grant number：RS2022A000613554  2022.09 - 2023.03

    塩野義製薬  奨学寄付サポート（Shionogi Academic support） 

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    Authorship：Principal investigator 

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  • 歯周病による胎児の成長阻害の分子メカニズム―『細胞外分泌小胞』の動態

    Grant number：MTPS20220624013  2022.09 - 2023.03

    田辺三菱製薬  田辺三菱医学薬学研究支援 (Mitsubishi Tanabe Pharma) 

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    Authorship：Principal investigator 

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  • Molecular mechanisms of the inhibition of placenta and fetus development induced by periodontal disease

    Grant number：22H03511  2022.04 - 2026.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    岡村 裕彦, 十川 千春, 江口 傑徳, 大森 一弘, 福原 瑶子, 池亀 美華

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    Grant amount：\17160000 （ Direct expense: \13200000 、 Indirect expense：\3960000 ）

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  • Molecular mechanisms of the inhibition of placenta and fetus development induced by periodontal disease

    Grant number：23K24768  2022.04 - 2026.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    岡村 裕彦, 十川 千春, 江口 傑徳, 大森 一弘, 池亀 美華, 福原 瑶子

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    Grant amount：\17160000 （ Direct expense: \13200000 、 Indirect expense：\3960000 ）

    胎盤は母体と胎児を結び，血液を介して栄養・代謝物，ガスの交換を行う精密な組織である。胎盤は小分子の通過を制御して母体の健康状態と胎児の成長発育において重要な役割を担っている。歯周病は口腔のみならず全身の健康状態に影響を及ぼす炎症性疾患である。妊娠中の母体が歯周病に罹患すると，母体の高血圧や腎臓・肝臓の機能障害などの疾患のみならず胎児の成長発育を阻害するが，その詳細な分子機構は分かっていなかった。我々は，歯周病原菌が感染したマクロファージ由来の『細胞外分泌小胞』が胎盤および胎児に移行し，著しい成長阻害を誘導することを見出した。そこで，『細胞外分泌小胞』の組織障害性とその動態に着目して，歯周病（原菌）が胎盤と胎児の成長を阻害する分子メカニズムを解明を目指した。
    歯周病原菌感染マクロファージ由来の『細胞外分泌小胞』を注入した妊娠マウスでは，胎盤と胎児の成長発育が著しく阻害された。この影響は，歯周病原菌本体を注入した場合の影響よりも強い傾向が認められた。『細胞外分泌小胞』は胎盤と胎児の成長発育に大きな影響を与える因子と考えられた。
    本年度は，歯周病原菌感染マクロファージ由来の『細胞外分泌小胞』を注入した妊娠マウスにおいて胎盤の血管構造の乱れが生じる要因について詳細に解析した。胎盤組織をホモジナイズし，蛋白質を抽出した。また，数ミリ角にした胎盤組織を培養液中で数時間培養し，その上清中に放出される『組織由来の細胞外分泌小胞』を回収する。これらのサンプルに含有される蛋白質の種類と量を世界最高水準の質量分析器を用いて網羅的に解析した（協力：がん研究会・植田幸嗣博士）。得られたデータについてプロテオミクス解析した。その結果，血管形成関連因子（VEGF, Angiogeninなど）に変動を認めた。

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  • A novel mechanism for promoting osteoblast differentiation by mechanical stimulation -- Function of transcription cofactor VGLL3

    Grant number：22K06790  2022.04 - 2025.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    池亀 美華, 岡村 裕彦, 平山 晴子, 福原 瑶子

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    Grant amount：\4030000 （ Direct expense: \3100000 、 Indirect expense：\930000 ）

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  • 母子健康に理想的な口腔環境を探る～歯周病原菌の小胞による胎盤組織への障害性～

    Grant number：21K19644  2021.07 - 2023.03

    日本学術振興会  科学研究費助成事業  挑戦的研究(萌芽)

    岡村 裕彦, 吉田 賀弥

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    Grant amount：\6500000 （ Direct expense: \5000000 、 Indirect expense：\1500000 ）

    胎盤は母体と胎児を結び，血液を介して栄養や代謝物，ガスの交換を行う精密な組織である。胎盤組織の恒常性は，母体の健康状態と胎児の成長発育に大きな影響を与え，その障害は，母体の高血圧症や肝臓・腎臓の機能障害，胎児の成長発育阻害に直結する。歯周病は歯周組織のみならず全身の健康状態に影響を及ぼす炎症性疾患である。妊娠中の母体が歯周病に罹患すると，母体の重篤な疾患や胎児の成長発育阻害を誘導する。そのため，歯周病（原菌）が胎盤組織にどのような障害を及ぼすかを明らかにすることは，母体の健康と胎児の成長発育に理想的な口腔環境を築くために重要である。
    我々は，歯周病原菌固有のDNAが胎盤組織で検出されたことから，菌由来のDNAや病原因子の胎盤への移行機序および胎盤組織の構造や機能への影響について解析を行っている。近年，我々は歯周病原菌が小さな分泌物を恒常的に放出し，生体側の細胞に様々な障害を及ぼすことを報告してきた。この分泌物は，『細胞外分泌小胞』と呼ばれ，細菌の外膜に由来する小胞で，内部には菌固有のDNAや病原因子を豊富に含んでいる。本研究では，歯周病原菌由来の『細胞外分泌小胞』の胎盤への移行とその障害性について解析を行い，歯周病が胎盤を介して母子の健康に与える影響とそのメカニズムを明らかにすることを目的としている。
    本年度は，妊娠マウスにおける『細胞外分泌小胞』の胎盤組織への移行について解析した。歯周病原菌由来の『細胞外分泌小胞』を蛍光標識し，妊娠マウスの尾静脈に投与し，胎盤への移行を調べた。胎盤および胎児において，赤色蛍光が検出された。また，検出される蛍光強度の強さと胎盤および胎児の形成障害の度合いとの間に関連性が示唆された。以上の結果より，歯周病原菌由来の『細胞外分泌小胞』は胎盤および胎児に移行することおよび形成を阻害することが明らかとなった。

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  • The liquid biopsy to detect the risk of multiple periodontal diseases associated-diseases

    Grant number：20K21714  2020.07 - 2022.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

    YOSHIDA Kaya

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    Grant amount：\5460000 （ Direct expense: \4200000 、 Indirect expense：\1260000 ）

    Periodontal diseases implicated in the pathology of many systemic diseases, such as diabetes mellitus, Alzheimer’s disease and rheumatic arthritis. In this study, we tried to provide the liquid biopsy which collectively detect the risk of many types of periodontal diseases associated diseases. The macrophages infected with Porphyromonas gingivalis were cultured under diabetes mellitus-like conditions. The exosomes were isolated from condition medium and microRNAs contained in exosomes were analyzed using microarray. We identified four microRNA species which increased by high glucose and AGE. The further investigations are needed to evaluate their potential as liquid biopsy for periodontal diseases associated diseases.

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  • The role of extracellular vesicles of oral bacteria in systemic disease

    Grant number：19H04051  2019.04 - 2023.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    岡村 裕彦, 江口 傑徳, 宝田 剛志, 吉田 賀弥, 池亀 美華, 江國 大輔, 伊原木 聰一郎

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    Grant amount：\17160000 （ Direct expense: \13200000 、 Indirect expense：\3960000 ）

    歯周病の病態の悪化が糖尿病などの全身性疾患の重症化に関与することが明らかになってきた。しかし，高齢者を中心に８割以上の人々が何らかの歯周疾患を患っており，深刻な国民的生活習慣病といえる。口腔は全身状態を示す鏡であり，健全な歯と口腔を維持することは，全身の健康にとって重要と認識されながらも，現状との間には依然として乖離がある。この原因として，歯周病と全身性疾患の重症化を関連づける明確な分子生物学的根拠が乏しいことが挙げられる。我々は，これらの疾患を関連づける新たな因子として歯周病原菌由来の『細胞外分泌小胞』を見出した。本研究では，歯周病原菌由来の『細胞外分泌小胞』に着目し，その成分と生体組織に対する障害性を調べ，歯周病および生活習慣病などの全身性疾患の早期診断への応用につなげることを目的とした。具体的には，1.歯周病原菌由来の『細胞外分泌小胞』の組織・細胞障害性を調べた。2.『細胞外分泌小胞』に含まれる病原因子を同定し，その細胞障害性について調べた。3.『細胞外分泌小胞』内の病原因子と歯周病および全身性疾患の病態との関連性を検討した。
    我々は，本研究を通して，世界で初めて歯周病原菌由来の『細胞外分泌小胞』を標識・可視化することに成功し，肝・腎・脳・肺など様々な臓器に移行することを見出した。また，歯周病原菌由来の『細胞外分泌小胞』は，１．肝臓に移行し肝細胞の糖代謝シグナルを阻害し糖尿病を悪化させること，２．肺の上皮細胞間の接着機構を破壊し細胞死を誘導すること，３．菌固有の病原因子である「ジンジパイン」を含むこと，を明らかにした。以上の研究成果により，歯周病原菌は，菌体から細胞外分泌小胞を放出することで，自らの病原因子を広範囲に拡散し，歯周組織や全身に障害を及ぼすことを明らかにした。

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  • Regulation of bone regeneration by exosomes and sugar chains derived from mechanical stress highly reactive mesenchymal stem cells

    Grant number：19K07269  2019.04 - 2022.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Ikegame Mika

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    Grant amount：\4420000 （ Direct expense: \3400000 、 Indirect expense：\1020000 ）

    We investigated the effect of exosomes secreted from preosteoblasts, on osteoblast differentiation and the effect of mechanical stress on the effect. As a result of adding exosomes obtained from the culture supernatant of the preosteoblast-like cell line (MC3T3-E1) to the osteoblast differentiation culture system, the expression of the osteoblast differentiation marker was suppressed. This effect was slightly strengthened in the exosomes from tensile-stressed cells. Therefore, it was suggested that exosomes produced from preosteoblasts have an osteoblast differentiation inhibitory effect, and that the inhibitory effect is enhanced by mechanical stress.

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  • Considering the effects of nerves on maxillofacial formation-elucidation of the etiology of hemifacial atrophy and hemifacial hypertrophy-

    Grant number：18K09832  2018.04 - 2021.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Kawanabe Noriaki

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    Grant amount：\4420000 （ Direct expense: \3400000 、 Indirect expense：\1020000 ）

    In this study, we conducted experiments to clarify the effects of the trigeminal nerve and facial nerve on the morphology of the maxillofacial region during growth. As a result of nerve activity blocking experiments and nerve activity activation experiments of the trigeminal nerve and facial nerve of rats, a decrease in the formation rate of cut teeth, calcification of the pulp, and disorder of the arrangement of ameloblasts and odontoblasts were observed. It was. In addition, as a result of analyzing Sonic hedgehog (Shh) gene-deficient mice and Shh gene-expressing mice, changes in bone and tooth morphology that are thought to be the effect of Shh on long-term maxillofacial morphogenesis were observed. As a result of conducting an experiment using fluorescence bioimaging, no characteristic stem cell dynamics were observed with or without nerve activity blocking / activation.

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  • 糖尿病重症化における「歯周病原菌由来の小さな分泌物」の役割

    2017.04 - 2018.03

    公益財団法人 鈴木謙三記念医科学応用研究財団  平成29年度調査研究助成金 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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  • 糖尿病重症化における歯周病原菌由来の細胞外分泌小胞の役割～微生物と細胞の新たなコミュニケーションツール～

    2017.04 - 2018.03

    The Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care  The Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care 

    OKAMURA Hirohiko

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    Authorship：Principal investigator  Grant type：Competitive

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  • The effects of PKR on progression of periodontal diseases-associated diabetes mellitus.

    Grant number：16K11506  2016.04 - 2019.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    YOSHIDA Kaya

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    Grant amount：\4550000 （ Direct expense: \3500000 、 Indirect expense：\1050000 ）

    We investigated whether Porphyromonas gingivalis (Pg) and AGEs affect bone metabolisms by regulating PKR activation. The treatment with Pg induced and activated PKR in mouse osteoblastic MC3T3-E1 cells. The high glucose conditions by treating with glucose increased the effects of Pg on PKR activation, whereas it induced no change of Pg internalization and morphology of osteoblasts. The PKR activated by Pg induced the differentiation of osteoblasts but not osteoclasts. These results suggested that high glucose conditions might be result in the inhibition of osteoblast differentiation by accelerating PKR under Pg infection.

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  • 骨芽細胞と脂肪細胞におけるPP2Aは互いの細胞分化を調節するか？

    2016.04 - 2017.03

    The Nakatomi Foundation  The Nakatomi Foundation 

    OKAMURA Hirohiko

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    Authorship：Principal investigator  Grant type：Competitive

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  • 口腔内細菌P. endodontalisによる歯槽骨吸収とヒストン脱メチル化酵素Jmjd3の役割

    2016.04 - 2017.03

    The Japan China Medical Association  The Japan China Medical Association 

    OKAMURA Hirohiko

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    Authorship：Principal investigator  Grant type：Competitive

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  • プロテインフォスファターゼ PP2A による骨形成と間葉系細胞分化機構の解明

    2014.04 - 2017.03

    日本学術振興会  日本学術振興会科学研究費 基盤研究 (C) 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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  • The effects of PKR and NLRP3 inflammasome on periodontal diseases

    Grant number：25462918  2013.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    YOSHIDA Kaya, OKAMURA Hirohiko

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    Grant amount：\4940000 （ Direct expense: \3800000 、 Indirect expense：\1140000 ）

    To investigate the roles of PKR and NLRP3 inflammasome on the progress of periodontal diseases, we examine whether PKR affect NLRP3 and bone metabolisms in P. gingivalis-infected osteoblasts.
    P. gingivalis increased the expression and phosphorylation of PKR in mouse osteoblasts, MC3T3-E1. P. gingivalis also induced and activated NLRP3, resulting in the increase of caspase-1 cleavage and interleukin (IL)-1b release. PKR was necessary to the up-regulation of NLRP3. Moreover, P. gingivalis affects the expression of several bone-related genes through by PKR-dependent pathway. These results showed that PKR mediates bone metabolisms by affecting NLRP3 and bone-related genes in periodontal diseases.

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  • The role of PKR on the differentiation of osteoblasts and formation of osteoclasts

    Grant number：25462859  2013.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    HANEJI Tatsuji, MORIMOTO Hiroyuki, TERAMACHI Jyumpei, OKAMURA Hirohiko

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    Grant amount：\5070000 （ Direct expense: \3900000 、 Indirect expense：\1170000 ）

    We investigated the roles of PKR in osteoclast formation and bone resorption in vitro and in vivo. LPS induced high levels of PKR in osteoclast precursor cells. The LPS-induced osteoclast differentiation was markedly suppressed in the cells pre-treated with PKR inhibitor, C16 and in the cells in which gene silencing of PKR were done. Inhibition of PKR activity in the cells was suppressed the expression of osteoclast differentiation markers including c-fos and NFATc. Bone resorption activity of the LPS-induced osteoclasts was also suppressed by the C16 treatment. Inhibition of PKR activity suppressed the LPS-induced activation of NF-κB and MAPK in osteoclasts. Treatment of C16 effectively prevented the LPS-induced destruction of alveolar bone in the artificial periodontitis in rat. Thus, the present results suggest that PKR plays a pivotal role in the LPS-induced bone loss in periodontitis and PKR inhibition may become an important therapeutic target for periodontitis.

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  • PP2A による骨芽-脂肪細胞間の相互作用と分化調節

    2013.04 - 2015.03

    Takeda Science Foundation  Takeda Science Foundation 

    OKAMURA Hirohiko

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    Authorship：Principal investigator  Grant type：Competitive

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  • Molecular characterization of the pathogenic factors of oral streptococci involved in autoimmune disease

    Grant number：24592833  2012.04 - 2015.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    HIROTA Katsuhiko, MIYAKE Yoichiro, MURAKAMI Keiji, OKAMURA Hirohiko

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    Grant amount：\5070000 （ Direct expense: \3900000 、 Indirect expense：\1170000 ）

    Using genome microarray to define the gene expression profile of rSi-HLP-stimulated THP-1 cells, 83 genes were up-regulated (two fold higher) among 28,869 genes profiled. Especially, genes coding for chemokines and pro-inflammatory cytokines, such as CCL2, 3, 4, CXCL8, 10 were the most highly up-regulated groups. Recombinant Streptococcus intermedius histone-like DNA binding protein is one of the set Inducer excessive CXCL10, CXCL 8, CCL2, CCL3, CCL4 from human THP-1 cells.

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  • プロテインフォスファターゼ PP2A による新たな骨芽細胞分化機構の解明

    2011.04 - 2014.03

    日本学術振興会  日本学術振興会科学研究費 基盤研究 (C) 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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  • PKRは骨芽細胞の悪性化に関与するか？

    2010.04 - 2011.03

    The Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care  The Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care 

    OKAMURA Hirohiko

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    Authorship：Principal investigator  Grant type：Competitive

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  • 骨芽細胞の分化におけるRNA Helicase A-Osterix相互作用の役割

    2008.04 - 2010.03

    日本学術振興会  日本学術振興会科学研究費 若手研究 (B) 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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  • RNA helicase Aの機能解明 －骨代謝調節を目指して－

    2007.04 - 2008.03

    科学技術振興機構  シーズ発掘試験 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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  • ヒストンH1.2による抗癌剤誘導アポトーシス促進機構

    2006.04 - 2008.03

    日本学術振興会  日本学術振興会科学研究費 若手研究 (B) 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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  • ブレオマイシン誘導アポトーシスにおけるヒストンH1.2とBak

    Grant number：18791382  2006 - 2007

    日本学術振興会  科学研究費助成事業  若手研究(B)

    岡村 裕彦

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    Grant amount：\3300000 （ Direct expense: \3300000 ）

    本研究では,抗癌剤ブレオマイシン(BLM)誘導アポトーシスとヒストンH1.2とミトコンドリア蛋白質であるBakの動向について詳細に検討を行った。その結果,
    1. BLMはヒストンH2AXのリン酸化とlamin B1 の分解を誘導した。
    2. BLM処理によりミトコンドリア膜障害が生じた。
    3. BLM処理細胞ではヒストンH1.2は核外に移行した。
    4. ヒストンH1.2はミトコンドリア上で,Bakと同様の局在を示した。
    BLMは,DNA傷害の後,ミトコンドリアからのチトクロムC放出,カスパーゼの活性によりアポトーシスを誘導する。この経路が進行するには核内でDNA傷害が生じたことを認識する分子,あるいは傷害を受けた分子そのものがミトコンドリアにその情報を伝えることが必要である。私は核クロマチン構成要素であるリンカーヒストンH1.2とミトコンドリアに局在するBc1-2ファミリー蛋白Bakに着目し解析を行った。H1.2は8種類のヒストンH1サブタイプの中で唯一チトクロムCの放出活性を持つ。Bakは抗癌剤を含む様々な刺激によりミトコンドリアからのチトクロムC放出を促進する。以上の所見は,ヒストンH1.2はDNA損傷後ミトコンドリアに移行し,Bakとの相互作用によりチトクロムCの放出を促進することを示している。今回はBLM処理細胞でヒストンH1.2とBakの時空間的な細胞内局在と他のアポトーシス関連現象について詳細に検討できた。これらの結果をまとめて,論文公表を行った(okamura, et. Al.,J Cell Biochem, 2008103(5):1488-96)

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  • Function of transcription factor in osteoblast

    2004

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    Grant type：Competitive

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  • 扁平上皮癌細胞の薬剤耐性と初期転写調節因子

    2003.04 - 2004.04

    日本学術振興会  特別研究員奨励費 

    岡村 裕彦

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    Authorship：Principal investigator  Grant type：Competitive

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