研究者詳細 - 米澤　朋子

論文 - 米澤　朋子

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Local E-rhBMP-2/β-TCP Application Rescues Osteocyte Dendritic Integrity and Reduces Microstructural Damage in Alveolar Bone Post-Extraction in MRONJ-like Mouse Model 査読

Anh Tuan Dang, Mitsuaki Ono, Ziyi Wang, Ikue Tosa, Emilio Satoshi Hara, Akihiro Mikai, Wakana Kitagawa, Tomoko Yonezawa, Takuo Kuboki, Toshitaka Oohashi

International Journal of Molecular Sciences 25 ( 12 ) 6648 - 6648 2024年6月

掲載種別：研究論文（学術雑誌）出版者・発行元：MDPI AG

The pathology of medication-related osteonecrosis of the jaw (MRONJ), often associated with antiresorptive therapy, is still not fully understood. Osteocyte networks are known to play a critical role in maintaining bone homeostasis and repair, but the exact condition of these networks in MRONJ is unknown. On the other hand, the local application of E-coli-derived Recombinant Human Bone Morphogenetic Protein 2/β-Tricalcium phosphate (E-rhBMP-2/β-TCP) has been shown to promote bone regeneration and mitigate osteonecrosis in MRONJ-like mouse models, indicating its potential therapeutic application for the treatment of MRONJ. However, the detailed effect of BMP-2 treatment on restoring bone integrity, including its osteocyte network, in an MRONJ condition remains unclear. Therefore, in the present study, by applying a scanning electron microscope (SEM) analysis and a 3D osteocyte network reconstruction workflow on the alveolar bone surrounding the tooth extraction socket of an MRONJ-like mouse model, we examined the effectiveness of BMP-2/β-TCP therapy on the alleviation of MRONJ-related bone necrosis with a particular focus on the osteocyte network and alveolar bone microstructure (microcrack accumulation). The 3D osteocyte dendritic analysis showed a significant decrease in osteocyte dendritic parameters along with a delay in bone remodeling in the MRONJ group compared to the healthy counterpart. The SEM analysis also revealed a notable increase in the number of microcracks in the alveolar bone surface in the MRONJ group compared to the healthy group. In contrast, all of those parameters were restored in the E-rhBMP-2/β-TCP-treated group to levels that were almost similar to those in the healthy group. In summary, our study reveals that MRONJ induces osteocyte network degradation and microcrack accumulation, while application of E-rhBMP-2/β-TCP can restore a compromised osteocyte network and abrogate microcrack accumulation in MRONJ.

DOI： 10.3390/ijms25126648

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Inverse genetics tracing the differentiation pathway of human chondrocytes 査読

H.T. Do, M. Ono, Z. Wang, W. Kitagawa, A.T. Dang, T. Yonezawa, T. Kuboki, T. Oohashi, S. Kubota

Osteoarthritis and Cartilage 2024年6月

Exploring the Regulators of Keratinization: Role of BMP-2 in Oral Mucosa 査読

Xindi Mu, Mitsuaki Ono, Ha Thi Thu Nguyen, Ziyi Wang, Kun Zhao, Taishi Komori, Tomoko Yonezawa, Takuo Kuboki, Toshitaka Oohashi

Cells 13 ( 10 ) 807 - 807 2024年5月

掲載種別：研究論文（学術雑誌）出版者・発行元：MDPI AG

The oral mucosa functions as a physico-chemical and immune barrier to external stimuli, and an adequate width of the keratinized mucosa around the teeth or implants is crucial to maintaining them in a healthy and stable condition. In this study, for the first time, bulk RNA-seq analysis was performed to explore the gene expression of laser microdissected epithelium and lamina propria from mice, aiming to investigate the differences between keratinized and non-keratinized oral mucosa. Based on the differentially expressed genes (DEGs) and Gene Ontology (GO) Enrichment Analysis, bone morphogenetic protein 2 (BMP-2) was identified to be a potential regulator of oral mucosal keratinization. Monoculture and epithelial–mesenchymal cell co-culture models in the air–liquid interface (ALI) indicated that BMP-2 has direct and positive effects on epithelial keratinization and proliferation. We further performed bulk RNA-seq of the ALI monoculture stimulated with BMP-2 in an attempt to identify the downstream factors promoting epithelial keratinization and proliferation. Analysis of the DEGs identified, among others, IGF2, ID1, LTBP1, LOX, SERPINE1, IL24, and MMP1 as key factors. In summary, these results revealed the involvement of a well-known growth factor responsible for bone development, BMP-2, in the mechanism of oral mucosal keratinization and proliferation, and pointed out the possible downstream genes involved in this mechanism.

DOI： 10.3390/cells13100807

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LCZ696 ameliorates doxorubicin-induced cardiomyocyte toxicity in rats. 査読国際誌

Toru Miyoshi, Kazufumi Nakamura, Naofumi Amioka, Omer F Hatipoglu, Tomoko Yonezawa, Yukihiro Saito, Masashi Yoshida, Satoshi Akagi, Hiroshi Ito

Scientific reports 12 ( 1 ) 4930 - 4930 2022年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

Doxorubicin (DOX)-based chemotherapy induces cardiotoxicity, which is considered the main bottleneck for its clinical application. In this study, we investigated the potential benefit of LCZ696, an angiotensin receptor-neprilysin inhibitor against DOX-induced cardiotoxicity in rats and H9c2 cells and determined whether the mechanism underlying any such effects involves its antioxidant activity. Male Sprague-Dawley rats were randomly separated into four groups, each consisting of 15 rats (DOX (1.5 mg/kg/day intraperitoneally for 10 days followed by non-treatment for 8 days); DOX + valsartan (31 mg/kg/day by gavage from day 1 to day 18); DOX + LCZ696 (68 mg/kg/day by gavage from day 1 to day 18); and control (saline intraperitoneally for 10 days). DOX-induced elevation of cardiac troponin T levels on day 18 was significantly reduced by LCZ696, but not valsartan. The DOX-induced increase in myocardial reactive oxygen species (ROS) levels determined using dihydroethidium was significantly ameliorated by LCZ696, but not valsartan, and was accompanied by the suppression of DOX-induced increase in p47phox. LCZ696 recovered the DOX-induced decrease in phosphorylation of adenosine monophosphate-activated protein kinase and increased the ratio of Bax and Bcl-2. In H9c2 cardiomyocytes, LCZ696 reduced DOX-induced mitochondrial ROS generation and improved cell viability more than valsartan. Our findings indicated that LCZ696 ameliorated DOX-induced cardiotoxicity in rat hearts in vivo and in vitro, possibly by mediating a decrease in oxidative stress.

DOI： 10.1038/s41598-022-09094-z

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Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic Aneurysms. 査読国際誌

Naofumi Amioka, Toru Miyoshi, Tomoko Yonezawa, Megumi Kondo, Satoshi Akagi, Masashi Yoshida, Yukihiro Saito, Kazufumi Nakamura, Hiroshi Ito

Frontiers in cardiovascular medicine 9 904215 - 904215 2022年

記述言語：英語掲載種別：研究論文（学術雑誌）

Background: Abdominal aortic aneurysm (AAA) is a life-threatening disease that lacks effective preventive therapies. This study aimed to evaluate the effect of pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPARα) agonist, on AAA formation and rupture. Methods: Experimental AAA was induced by subcutaneous angiotensin II (AngII) infusion in ApoE - / - mice for 4 weeks. Pemafibrate (0.1 mg/kg/day) was administered orally. Dihydroethidium staining was used to evaluate the reactive oxygen species (ROS). Results: The size of the AngII-induced AAA did not differ between pemafibrate- and vehicle-treated groups. However, a decreased mortality rate due to AAA rupture was observed in pemafibrate-treated mice. Pemafibrate ameliorated AngII-induced ROS and reduced the mRNA expression of interleukin-6 and tumor necrosis factor-α in the aortic wall. Gelatin zymography analysis demonstrated significant inhibition of matrix metalloproteinase-2 activity by pemafibrate. AngII-induced ROS production in human vascular smooth muscle cells was inhibited by pre-treatment with pemafibrate and was accompanied by an increase in catalase activity. Small interfering RNA-mediated knockdown of catalase or PPARα significantly attenuated the anti-oxidative effect of pemafibrate. Conclusion: Pemafibrate prevented AAA rupture in a murine model, concomitant with reduced ROS, inflammation, and extracellular matrix degradation in the aortic wall. The protective effect against AAA rupture was partly mediated by the anti-oxidative effect of catalase induced by pemafibrate in the smooth muscle cells.

DOI： 10.3389/fcvm.2022.904215

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Protective Role of Limitrin in Experimental Autoimmune Optic Neuritis 査読国際共著国際誌

Bo Young Chun, Jong-Heon Kim, Youn-Kwan Jung, Yoon Seok Choi, Gunwoo Kim, Tomoko Yonezawa, Kyoungho Suk

Investigative Opthalmology & Visual Science 62 ( 9 ) 8 - 8 2021年7月

Lack of collagen α6(IV) chain in mice does not cause severe-to-profound hearing loss or cochlear malformation, a distinct phenotype from nonsyndromic hearing loss with COL4A6 missense mutation. 査読国際誌

Shaoying Tang, Tomoko Yonezawa, Yukihide Maeda, Mitsuaki Ono, Takahiro Maeba, Toru Miyoshi, Ryusuke Momota, Yasuko Tomono, Toshitaka Oohashi

PloS one 16 ( 4 ) e0249909 - e0249909 2021年4月

担当区分：責任著者記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Public Library of Science (PLoS)

Congenital hearing loss affects 1 in every 1000 births, with genetic mutations contributing to more than 50% of all cases. X-linked nonsyndromic hereditary hearing loss is associated with six loci (DFNX1-6) and five genes. Recently, the missense mutation (c.1771G>A, p.Gly591Ser) in <italic>COL4A6</italic>, encoding the basement membrane (BM) collagen α6(IV) chain, was shown to be associated with X-linked congenital nonsyndromic hearing loss with cochlear malformation. However, the mechanism by which the <italic>COL4A6</italic> mutation impacts hereditary hearing loss has not yet been elucidated. Herein, we investigated <italic>Col4a6</italic> knockout (KO) effects on hearing function and cochlear formation in mice. Immunohistochemistry showed that the collagen α6(IV) chain was distributed throughout the mouse cochlea within subepithelial BMs underlying the interdental cells, inner sulcus cells, basilar membrane, outer sulcus cells, root cells, Reissner’s membrane, and perivascular BMs in the spiral limbus, spiral ligament, and stria vascularis. However, the click-evoked auditory brainstem response analysis did not show significant changes in the hearing threshold of <italic>Col4a6</italic> KO mice compared with wild-type (WT) mice with the same genetic background. In addition, the cochlear structures of <italic>Col4a6</italic> KO mice did not exhibit morphological alterations, according to the results of high-resolution micro-computed tomography and histology. Hence, loss of <italic>Col4a6</italic> gene expression in mice showed normal click ABR thresholds and normal cochlear formation, which differs from humans with the <italic>COL4A6</italic> missense mutation c.1771G>A, p.Gly591Ser. Therefore, the deleterious effects in the auditory system caused by the missense mutation in <italic>COL4A6</italic> are likely due to the dominant-negative effects of the α6(IV) chain and/or α5α6α5(IV) heterotrimer with an aberrant structure that would not occur in cases with loss of gene expression.

DOI： 10.1371/journal.pone.0249909

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Deficiency of CD44 prevents thoracic aortic dissection in a murine model. 査読国際誌

Omer F Hatipoglu, Toru Miyoshi, Tomoko Yonezawa, Megumi Kondo, Naofumi Amioka, Masashi Yoshida, Satoshi Akagi, Kazufumi Nakamura, Satoshi Hirohata, Hiroshi Ito

Scientific reports 10 ( 1 ) 6869 - 6869 2020年4月

記述言語：英語掲載種別：研究論文（学術雑誌）

Thoracic aortic dissection (TAD) is a life-threatening vascular disease. We showed that CD44, a widely distributed cell surface adhesion molecule, has an important role in inflammation. In this study, we examined the role of CD44 in the development of TAD. TAD was induced by the continuous infusion of β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, and angiotensin II (AngII) for 7 days in wild type (WT) mice and CD44 deficient (CD44-/-) mice. The incidence of TAD in CD44-/- mice was significantly reduced compared with WT mice (44% and 6%, p < 0.01). Next, to evaluate the initial changes, aortic tissues at 24 hours after BAPN/AngII infusion were examined. Neutrophil accumulation into thoracic aortic adventitia in CD44-/- mice was significantly decreased compared with that in WT mice (5.7 ± 0.3% and 1.6 ± 0.4%, p < 0.01). In addition, BAPN/AngII induced interleukin-6, interleukin-1β, matrix metalloproteinase-2 and matrix metalloproteinase-9 in WT mice, all of which were significantly reduced in CD44-/- mice (all p < 0.01). In vitro transmigration of neutrophils from CD44-/- mice through an endothelial monolayer was significantly decreased by 18% compared with WT mice (p < 0.01). Our findings indicate that CD44 has a critical role in TAD development in association with neutrophil infiltration into adventitia.

DOI： 10.1038/s41598-020-63824-9

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細胞外基質が細胞遊走に及ぼす影響の評価を目的とした細胞遊走アッセイ

塩出雄亮, 森實祐基, 平野雅幸, 土居真一郎, 戸島慎二, 荒木亮一, 高橋耕介, 松前洋, 神崎勇希, 細木三佳, 米澤朋子, 白神史雄

日本眼科学会雑誌 122 ( 臨増 ) 226 - 226 2018年3月

剥離した内境界膜に含まれる終末糖化産物の定量評価

的場亮, 森實祐基, 木村修平, 米澤朋子, 須野学, 岡野内俊雄, 高畠隆, 三原研一, 佐々木ミチ, 飯島克昌, 白神史雄

日本眼科学会雑誌 120 ( 臨増 ) 185 - 185 2016年3月

ミュラー細胞の増殖、遊走における4型コラーゲンの役割

塩出雄亮, 森實祐基, 的場亮, 平野雅幸, 土居真一郎, 荒木亮一, 米澤朋子, 白神史雄

日本眼科学会雑誌 119 ( 臨増 ) 168 - 168 2015年3月

ARPE-19の細胞増殖におけるAMP依存性キナーゼの役割

塚本真啓, 木村修平, 米澤朋子, 小阪淳, 森實祐基

日本眼科学会雑誌 117 ( 臨増 ) 352 - 352 2013年3月

Distribution of alpha(IV) collagen chains in the ocular anterior segments of adult mice 査読

Kenji Saito, Tomoko Yonezawa, Jun Minaguchi, Masae Kurosaki, Shiho Suetsugu, Ai Nakajima, Hiroyuki Nomoto, Yuki Morizane, Yoshikazu Sado, Manabu Sugimoto, Shozo Kusachi, Yoshifumi Ninomiya

CONNECTIVE TISSUE RESEARCH 52 ( 2 ) 147 - 156 2011年4月

担当区分：責任著者記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：INFORMA HEALTHCARE

The distribution of the collagen chains from alpha 1(IV) to alpha 6(IV) could serve as a basis for the characterization of type IV collagen. In this study, immunohistochemistry of the ocular anterior segment of adult mice was performed using specific monoclonal antibodies against each chain in the series from alpha 1(IV) to alpha 6(IV). The results show that the components of type IV collagen in vascular basement membranes are alpha 1(IV) and alpha 2(IV) with or without alpha 5(IV) and alpha 6(IV) chains and those in epithelium and muscle basement membranes are alpha 1(IV), alpha 2(IV), alpha 5(IV), and alpha 6(IV) chains. In corneal endothelium, pigmented epithelium of iris and ciliary body, and trabecular meshwork, alpha 3(IV) and alpha 4(IV) chains are also expressed in addition to alpha 1(IV), alpha 2(IV), alpha 5(IV), and alpha 6(IV) chains. Moreover, we investigated the change in molecular composition in ciliary body during postnatal development. alpha 3(IV) and alpha 4(IV) chains were also expressed in addition to alpha 1(IV), alpha 2(IV), alpha 5(IV), and alpha 6(IV) chains in ciliary pigmented epithelium basement membrane from 7 days after birth. This result suggests that the basement membranes gradually change their biochemical features owing to temporal regulation. Taken together, these findings suggest that the different distribution and the developmental expression of alpha 1(IV) to alpha 6(IV) chains are associated with the tissue-specific function of type IV collagen in basement membranes.

DOI： 10.3109/03008207.2010.492062

Web of Science

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Tumor-specific expression of the RGD-alpha3(IV)NC1 domain suppresses endothelial tube formation and tumor growth in mice. 査読

Miyoshi T, Hirohata S, Ogawa H, Doi M, Obika M, Yonezawa T, Sado Y, Kusachi S, Kyo S, Kondo S, Shiratori Y, Hudson BG, Ninomiya Y

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20 ( 11 ) 1904 - 1906 2006年9月

ヒト皮膚および付属器の基底膜IV型コラーゲンα鎖構成

長谷川治子, 内藤一郎, 中野和代, 米澤朋子, 西田圭一郎, 田口勇仁, 佐渡義一, 二宮善文, 大塚愛二

解剖学雑誌 80 ( 1 ) 20 - 20 2005年3月

ヒト皮膚とその付属器の基底膜を構成するIV型コラーゲン分子のα鎖構成

長谷川治子, 内藤一郎, 中野和代, 米澤朋子, 西田圭一郎, 田口勇仁, 佐渡義一, 二宮善文, 大塚愛二

解剖学雑誌 80 ( Suppl. ) 151 - 151 2005年3月

Limitrin, a Novel Immunoglobulin Superfamily Protein Localized to Glia Limitans Formed by Astrocyte Endfeet 査読

Tomoko Yonezawa, Aiji Ohtsuka, Teruhito Yoshitaka, Shuichi Hirano, Hiroyuki Nomoto, Kiyotaka Yamamoto, Yoshifumi Ninomiya

GLIA 44 ( 3 ) 190 - 204 2003年12月

担当区分：筆頭著者記述言語：英語掲載種別：研究論文（学術雑誌）

We report the molecular cloning of a new member of the transmembrane-type immunoglobulin superfamily and designate the encoded protein as limitrin, since it localized selectively to glia limitans in mouse brain. Limitrin cDNA was obtained using a subtractive hybridization procedure designed to identify molecules responsible for blood-brain barrier function. Western blots using a limitrin-specific antibody demonstrated that the gene product is expressed significantly in mouse brain and primary murine astrocytes and is distributed in the plasma membrane. Immunohistochemical studies using confocal and electron microscopy clearly demonstrated highly polarized localization in astroglial endfeet in the perivascular region and under the pia mater in vivo. Limitrin is expressed in the spinal cord and in many areas of the brain, but not in the median eminence or subfornical organ (the circumventricular organs), where the blood-brain barrier is lacking. Disruption of the blood-brain barrier by cold injury resulted in a drastic reduction in limitrin expression. Furthermore, during retrieval from cold injury, the increased expression of limitrin in perivascular endfeet correlated with the recovery of angiogenesis in capillaries within the lesion margins. Our results suggest that limitrin is physically and functionally associated with the blood-brain barrier, implying that this protein may be useful as a diagnostic tool of barrier integrity. © 2003 Wiley-Liss, Inc.

DOI： 10.1002/glia.10279

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