Updated on 2022/09/21

写真a

 
IZAWA Takashi
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Associate Professor
Position
Associate Professor
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Degree

  • Ph.D. ( 2004.3   The University of Tokushima )

Research Interests

  • Medical-Engineering Cooperation

  • Challenging and Exploratory Research

  • Orthodontics

  • Rheumatoid Arthritis

  • coupling factor

  • osteoclast

  • 骨転移性癌

  • 国際共同研究強化

  • Rare Disease

  • Pathology and Immunology

  • 骨免疫学

  • Osteoimmunology

Research Areas

  • Life Science / Developmental dentistry

Education

  • The University of Tokushima   歯学研究科   博士課程 修了

    - 2004

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    Country: Japan

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  • The University of Tokushima    

    - 2004

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  • The University of Tokushima    

    - 2000

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  • The University of Tokushima   歯学部   歯学科 卒業

    - 2000

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    Country: Japan

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Research History

  • Okayama University   Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences   Associate Professor

    2021.9

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  • Okayama University   Hospital, Orthodontics   Lecturer

    2019.10 - 2021.8

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  • Tokushima University Graduate School, Institute of Biomedical Sciences   Department of Orthodontics and Dentofacial Orthopedics   Assistant Professor

    2015.4 - 2019.9

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  • University of Tokushima Graduate School, Institute for Health Bioscience   Department of Orthodontics and Dentofacial Orthopedics   Assistant Professor

    2012.10 - 2015.3

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  • Washington University in St. Louis, School of Medicine   Department of Pathology and Immunology   Postdoc Research Associate

    2009.10 - 2012.9

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  • University of Tokushima Graduate School, Institute for Health Bioscience   Department of Orthodontics and Dentofacial Orthopedics   Research Assistant

    2004.4 - 2009.9

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Professional Memberships

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Committee Memberships

  • 日本矯正歯科学会   代議員  

    2022.4   

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  • Chu-shikoku orthodontic society   Council  

    2022.1   

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    Committee type:Academic society

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  •   令和3年度岡山大学未来懇談会参加メンバー  

    2021.11 - 2022.3   

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    Committee type:Other

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  • 岡山歯学会   評議員  

    2021.8   

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    Committee type:Other

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  • Chu-shikoku orthodontic society   spare council  

    2020.4 - 2021.7   

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    Committee type:Academic society

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  • 徳島大学研究クラスター   選定クラスター (#1803001) クラスター長  

    2018.8 - 2019.3   

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    Committee type:Academic society

    https://cluster.tokushima-u.ac.jp/news/912.html

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  • 四国歯学会   評議員  

    2018.4 - 2019.9   

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  • 中・四国矯正歯科学会   学術理事(学術委員長)  

    2018.1 - 2019.12   

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    Committee type:Academic society

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  • 中・四国矯正歯科学会   学術委員  

    2013.4 - 2017.12   

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    Committee type:Academic society

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  • 日本矯正歯科学会   代議員  

    2008.4 - 2010.3   

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  • 中・四国矯正歯科学会   編集幹事  

    2008.4 - 2009.12   

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Papers

  • HIF‐1α controls palatal wound healing by regulating macrophage motility via S1P/S1P 1 signaling axis Reviewed

    Islamy Rahma Hutami, Takashi Izawa, Tsendsuren Khurel‐Ochir, Takuma Sakamaki, Akihiko Iwasa, Shuhei Tomita, Eiji Tanaka

    Oral Diseases   28 ( 4 )   1157 - 1169   2022.5

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

    DOI: 10.1111/odi.13856

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1111/odi.13856

  • ThPOK inhibits osteoclast formation via NFATc1 transcription and function Reviewed International coauthorship International journal

    Wei Zou, Takashi Izawa, Nidhi Rohatgi, Steven Y Zou, Yongjia Li, Steven L Teitelbaum

    JBMR Plus   6 ( 4 )   e10613   2022.3

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    DOI: 10.1002/jbm4.10613

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

    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   47 ( 6 )   992 - 1015   2021.8

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    This study aimed to reveal the possible mechanisms by which O-linked-N-acetylglucosaminylation (O-GlcNAcylation) regulates osteoblast differentiation using a series of bioinformatics-oriented experiments. To examine the influence of O-GlcNAcylation levels on osteoblast differentiation, osteoblastic MC3T3-E1 cells were treated with O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) inhibitors. Correlations between the levels of O-GlcNAcylation and the expression of osteogenic markers as well as OGT were evaluated by qPCR and western blotting. The O-GlcNAcylated proteins assumed to correlate with Runx2 expression were retrieved from several public databases and used for further bioinformatics analysis. Following the findings of the bioinformatics analysis, intracellular calcium ([Ca2+ ]i ) was monitored in the cells treated with OGT and OGA inhibitors using a confocal laser-scanning microscope (CLS). The interaction effect between O-GlcNAcylation and [Ca2+ ]i on osteogenic marker expression was determined using stable OGT knockdown MC3T3-E1 cells. O-GlcNAcylation was positively associated with osteoblast differentiation. The time-course profile of global O-GlcNAcylated proteins showed a distinctive pattern with different molecular weights during osteoblast differentiation. The expression pattern of several O-GlcNAcylated proteins was significantly similar to that of Runx2 expression. Bioinformatic analysis of the retrieved Runx2-related-O-GlcNAcylated-proteins revealed the importance of [Ca2+ ]i . CLS showed that alteration of O-GlcNAcylation rapidly changed [Ca2+ ]i in MC3T3-E1 cells. O-GlcNAcylation and [Ca2+ ]i showed an interaction effect on the expression of osteogenic markers. OGT knockdown disrupted the [Ca2+ ]i -induced expression changes of osteogenic markers. O-GlcNAcylation interacts with [Ca2+ ]i and elicits osteoblast differentiation by regulating the expression of osteogenic markers.

    DOI: 10.1002/biof.1774

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

  • Macrophage Motility in Wound Healing Is Regulated by HIF-1a via S1P Signaling Reviewed

    Islamy Rahma Hutami, Takashi Izawa, Tsendsuren Khurel-Ochir, Takuma Sakamaki, Akihiko Iwasa, Eiji Tanaka

    International Journal of Molecular Sciences   22 ( 16 )   8992 - 8992   2021.8

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

    Accumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, inflammation. Hypoxic conditions generated at a wound site also strongly recruit macrophages and affect their function. Hypoxia inducible factor (HIF)-1α is a transcription factor that contributes to both glycolysis and the induction of inflammatory genes, while also being critical for macrophage activation. For the latter, HIF-1a regulates sphingosine 1-phosphate (S1P) to affect the migration, activation, differentiation, and polarization of macrophages. Recently, S1P and HIF-1α have received much attention, and various studies have been performed to investigate their roles in initiating and resolving inflammation via macrophages. It is hypothesized that the HIF-1α/S1P/S1P receptor axis is an important determinant of macrophage function under inflammatory conditions and during disease pathogenesis. Therefore, in this review, biological regulation of monocytes/macrophages in response to circulating HIF-1α is summarized, including signaling by S1P/S1P receptors, which have essential roles in wound healing.

    DOI: 10.3390/ijms22168992

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  • Roles for B[a]P and FICZ in subchondral bone metabolism and experimental temporomandibular joint osteoarthritis via the AhR/Cyp1a1 signaling axis Reviewed

    Yuri Yoshikawa, Takashi Izawa, Yusaku Hamada, Hiroko Takenaga, Ziyi Wang, Naozumi Ishimaru, Hiroshi Kamioka

    Scientific Reports   11 ( 1 )   14927   2021.7

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    <title>Abstract</title>Bone loss due to smoking represents a major risk factor for fractures and bone osteoporosis. Signaling through the aryl hydrocarbon receptor (AhR) and its ligands contributes to both bone homeostasis and inflammatory diseases. It remains unclear whether the same AhR signaling axis affects the temporomandibular joint (TMJ). The aim of this study was to investigate possible mechanisms which mediate bone loss in the TMJ due to smoking. In particular, whether benzo[<italic>a</italic>]pyrene (B[<italic>a</italic>]P), a carcinogen of tobacco smoke, induces expression of the AhR target gene, Cyp1a1, in mandibular condyles. Possible functions of an endogenous ligand of FICZ, were also investigated in a TMJ-osteoarthritis (OA) mouse model. B[<italic>a</italic>]P was administered orally to wild-type and <italic>AhR</italic>−/− mice and bone metabolism was subsequently examined. TMJ-OA was induced in wild-type mice with forceful opening of the mouth. Therapeutic functions of FICZ were detected with μCT and histology. Exposure to B[<italic>a</italic>]P accelerated bone loss in the mandibular subchondral bone. This bone loss manifested with osteoclastic bone resorption and upregulated expression of Cyp1a1 in an <italic>AhR</italic>-dependent manner. In a mouse model of TMJ-OA, FICZ exhibited a dose-dependent rescue of mandibular subchondral bone loss by repressing osteoclast activity. Meanwhile, in vitro, pre-treatment with FICZ reduced RANKL-mediated osteoclastogenesis. B[<italic>a</italic>]P regulates mandibular subchondral bone metabolism via the Cyp1a1. The AhR ligand, FICZ, can prevent TMJ-OA by regulating osteoclast differentiation.

    DOI: 10.1038/s41598-021-94470-4

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    Other Link: http://www.nature.com/articles/s41598-021-94470-4

  • The immunoregulatory role of p21 in the development of the temporomandibular joint‐osteoarthritis Reviewed

    Tsendsuren Khurel‐Ochir, Takashi Izawa, Akihiko Iwasa, Fumiya Kano, Akihito Yamamoto, Eiji Tanaka

    Clinical and Experimental Dental Research   7 ( 3 )   313 - 322   2021.6

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    DOI: 10.1002/cre2.404

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    Other Link: https://onlinelibrary.wiley.com/doi/full-xml/10.1002/cre2.404

  • Case report Reviewed

    The Journal of Okayama Dental Society   40 ( 1 )   1 - 10   2021.6

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    Language:Japanese  

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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 International journal

    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>
    <sec>
    <title>Methods</title>
    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>
    <sec>
    <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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    DOI: 10.7717/peerj.10244

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    Other Link: https://peerj.com/articles/10244.xml

  • Skeletal open bite with amelogenesis imperfecta treated with compression osteogenesis: a case report. Reviewed

    Mori H, Izawa T, Mori H, Watanabe K, Kanno T, Tanaka E

    Head Face Med   15 ( 1 )   3   2019.1

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    DOI: 10.1186/s13005-019-0187-7.

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  • Crosstalk between Fas and S1P1 signaling via NF-kB in osteoclasts controls bone destruction in the TMJ due to rheumatoid arthritis Reviewed

    Hutami IR, Tanaka E, Izawa T

    Japanese Dental Science Review   55 ( 1 )   12 - 19   2019.1

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    DOI: 10.1016/j.jdsr.2018.09.004

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  • Clinico-statistical survey for congenital missing of permanent teeth in orthodontic patients Reviewed

    Ogasawara Naoko, Iwasa Akihiko, Shinya Horiuchi, Izawa Takashi

    THE JOURNAL OF CHU-SHIKOKU ORTHODONTIC SOCIETY   30 ( 1 )   59 - 64   2018.8

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  • Effectiveness of presurgical nasoalveolar molding therapy on unilateral cleft lip nasal deformity Reviewed

    Nao Kinouchi, Shinya Horiuchi, Akihiro Yasue, Yuko Kuroda, Nobuhiko Kawai, Keiichiro Watanabe, Takashi Izawa, Ichiro Hashimoto, Ali H. Hassan, Eiji Tanaka

    Saudi Medical Journal   39 ( 2 )   169 - 178   2018.2

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    Objectives: To evaluate the effectiveness of pre-surgical nasoalveolar molding (PNAM) in patients with unilateral cleft lip nasal deformities. Methods: This was a retrospective study involving 29 patients with unilateral cleft lip and palate defects, of whom 13 were treated with palatal devices with nasal stents (PNAM group) and 16 were treated with palatal devices without nasal stents or surgical tapes (control group). Submental oblique photographs and orthodontic models were longitudinally obtained at the initial visit (T1) and immediately before (T2) and after cheiloplasty (T3). Asymmetry of the external nose, degree of columellar shifting, nasal tip/ala nose ratio, nasal base angle, interalveolar gap, and the sagittal difference in the alveolar gap were measured. The study was conducted in the Orthodontic Clinic at Tokushima University Hospital, Tokushima, Japan between 1997 and 2012. Results: At T1, there were no significant intergroup differences in the first 4 asymmetry parameters. At T2, the PNAM group showed a significant improvement in all values compared to the control group. At T3, the PNAM group showed significant improvement in nasal asymmetry and columellar shifting. Model analysis showed significantly greater changes in the inter-alveolar gap and the sagittal difference of the alveolar cleft gap from T1 to T2 in the PNAM group. Conclusion: The use of PNAM is indispensable for pre-surgical orthodontic treatment at the early postnatal age.

    DOI: 10.15537/smj.2018.2.21020

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  • Potential role of rebamipide in osteoclast differentiation and mandibular condylar cartilage homeostasis Reviewed

    Takashi Izawa, Islamy Rahma Hutami, Eiji Tanaka

    Current Rheumatology Reviews   14 ( 1 )   62 - 69   2018

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Bentham Science Publishers B.V.  

    Background: Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease that involves changes in subchondral bone and progressive degradation of cartilage. Currently, rebamipide, a gastroprotective drug, is administered to protect gastric mucosa and accelerate ulcer healing. Objectives: Recent studies have shown that rebamipide also attenuates cartilage degeneration by suppressing oxidative damage and inducing homeostasis of the extracellular matrix of articular chondrocytes. Regarding the latter, reduced expression of cathepsin K, NFATc1, c-Src, and integrin β3, and increased expression of nuclear factor-kappa B, have been found to be mediated by the transcription factor, receptor activator of nuclear factor kappa-B ligand (RANKL). Methods: Treatment with rebamipide was also found to activate, mitogen-activated protein kinases such as p38, ERK, and JNK to reduce osteoclast differentiation. Taken together, these results strongly indicate that rebamipide mediates inhibitory effects on cartilage degradation and osteoclastogenesis in TMJ-OA. Results and Conclusion: Here, we highlight recent evidence regarding the potential for rebamipide to affect osteoclast differentiation and TMJ-OA pathogenesis. We also discuss the potential role of rebamipide to serve as a new strategy for the treatment of TMJ-OA.

    DOI: 10.2174/1573397113666171017113441

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  • Skeletal anchorage for intrusion of bimaxillary molars in a patient with skeletal open bite and temporomandibular disoeders. Reviewed

    Iwasa A, Horiuchi S, Kinouchi N, Izawa T, Hiasa M, Kawai N, Yasue A, Hassan AH, Tanaka E

    Journal of Orthodontic Science   6 ( 4 )   152 - 158   2017.10

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    DOI: 10.4103/jos.JOS_63_17

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  • Fas/S1P(1) crosstalk via NF-kappa B activation in osteoclasts controls subchondral bone remodeling in murine TMJ arthritis Reviewed

    Islamy Rahma Hutami, Takashi Izawa, Akiko Mino-Oka, Takehiro Shinohara, Hiroki Mori, Akihiko Iwasa, Eiji Tanaka

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   490 ( 4 )   1274 - 1281   2017.9

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Enhanced turnover of subchondral trabecular bone is a hallmark of rheumatoid arthritis (RA) and it results from an imbalance between bone resorption and bone formation activities. To investigate the formation and activation of osteoclasts which mediate bone resorption, a Fas-deficient MRL/Ipr mouse model which spontaneously develops autoimmune arthritis and exhibits decreased bone mass was studied. Various assays were performed on subchondral trabecular bone of the temporomandibular joint (TMJ) from MRL/lpr mice and MRL+/+ mice. Initially, greater osteoclast production was observed in vitro from bone marrow macrophages obtained from MRL/lpr mice due to enhanced phosphorylation of NF-kappa B, as well as Akt and MAPK, to receptor activator of nuclear factor-kappa B ligand (RANKL). Expression of sphingosine 1-phosphate receptor 1 (SIP1) was also significantly upregulated in the condylar cartilage. S1P(1) was found to be required for S1P-induced migration of osteoclast precursor cells and downstream signaling via Rac1. When SN50, a synthetic NF-kappa B-inhibitory peptide, was applied to the MRL/Ipr mice, subchondral trabecular bone loss was reduced and both production of osteoclastogenesis markers and sphingosine kinase (Sphk) 1/S1P(1) signaling were reduced. Thus, the present results suggest that Fas/S1P(1) signaling via activation of NF-kappa B in osteoclast precursor cells is a key factor in the pathogenesis of RA in the TMJ. (C) 2017 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2017.07.006

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  • Role of Fas and RANKL signaling in peripheral immune tolerance Reviewed

    Izawa T, Arakaki R, Ishimaru N

    Journal of Clinical & Cellular Immunology   8 ( 4 )   512   2017.7

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

    DOI: 10.4172/2155-9899.1000512

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  • Role of Smad3 and S1P signal in mandibular condylar cartilage homeostasis Reviewed

    Izawa T, Hutami IR, Mori H, Tanaka E

    Journal of Bone Research   5 ( 2 )   178 - 178   2017.7

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    DOI: 10.4172/2572-4916.100017

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  • Crosstalk between cytokine RANKL and AhR signalling in osteoclasts controls bone homeostasis Reviewed

    Izawa T, Arakaki R, Ishimaru N

    Journal of Cytokine Biology   2 ( 2 )   114   2017.5

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    DOI: 10.4172/2576-3881.1000114

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  • Long-term follow-up of a patient with achondroplasia treated with an orthodontic approach Reviewed

    Hiroyo Mori, Kazuma Matsumoto, Nobuhiko Kawai, Takashi Izawa, Shinya Horiuchi, Eiji Tanaka

    AMERICAN JOURNAL OF ORTHODONTICS AND DENTOFACIAL ORTHOPEDICS   151 ( 4 )   793 - 803   2017.4

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:MOSBY-ELSEVIER  

    We successfully treated a patient with achondroplasia with conventional orthodontic techniques. It was followed by long-term retention. The patient, a 12-year-old boy, had chief complaints of occlusal disturbance and mandibular protrusion. He had been diagnosed with achondroplasia and had growth hormone treatment in his early teenage years. His facial profile was concave with a bulging forehead and a retrognathic maxilla. It was characterized by a skeletal Class III jaw-base relationship with a retropositioned maxilla. At the age of 12 years 9 months, maxillary protraction was initiated with a reverse headgear; for 2 years 6 months, the maxillomandibular growth was controlled. After the growth spurt, at the age of 15 years 6 months, leveling and alignment of both dental arches were started with preadjusted edgewise appliances. After 83 months of multibracket treatment, an acceptable occlusion with a Class I molar relationship and an adequate interincisal relationship was achieved, despite the simultaneous marked vertical growth of the mandible. The resultant occlusion was stable during a 6-year retention period, although considerable forward-downward mandibular growth was observed. Conclusively, our results indicated the necessity of long-term observation in this patient with achondroplasia, especially because of the persistent mandibular growth.

    DOI: 10.1016/j.ajodo.2016.03.034

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  • Roles of hypoxia inducible factor-1 alpha in the temporomandibular joint Reviewed

    Akiko Mino-Oka, Takashi Izawa, Takehiro Shinohara, Hiroki Mori, Akihiro Yasue, Shuhei Tomita, Eiji Tanaka

    ARCHIVES OF ORAL BIOLOGY   73   274 - 281   2017.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:PERGAMON-ELSEVIER SCIENCE LTD  

    Objective: Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease characterized by permanent cartilage loss. Articular cartilage is maintained in a low-oxygen environment. The chondrocyte response to hypoxic conditions involves expression of hypoxia inducible factor 1 alpha (HIF-1 alpha), which induces chondrocytes to increase expression of vascular endothelial growth factor (VEGF). Here, we investigated the role of HIF-1 alpha in mechanical load effects on condylar cartilage and subchondral bone in heterozygous HIF-1 alpha-deficient mice (HIF-1 alpha(+/-)).
    Design: Mechanical stress was applied to the TMJ of C57BL/6NCr wild-type (WT) and HIF-1 alpha(+/-) mice with a sliding plate for 10 days. Histological analysis was performed by HE staining, Safranin-O/Fast green staining, and immunostaining specific for articular cartilage homeostasis.
    Results: HIF-1 alpha+/- mice had thinner cartilage and smaller areas of proteoglycan than WT controls, without and with mechanical stress. Mechanical stress resulted in prominent degenerative changes with increased expression of HIF-1 alpha, VEGF, and the apoptosis factor cleaved Caspase-3 in condylar cartilage.
    Conclusion: Our results indicate that HIF-1 alpha may be important for articular cartilage homeostasis and protective against articular cartilage degradation in the TMJ under mechanical stress condition, therefore HIF-1 alpha could be an important new therapeutic target in TMJ-OA. (C) 2016 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.archoralbio.2016.10.028

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  • Hyaluronan metabolism in overloaded temporomandibular joint Reviewed

    T. Shinohara, T. Izawa, A. Mino-Oka, H. Mori, A. Iwasa, T. Inubushi, Y. Yamaguchi, E. Tanaka

    JOURNAL OF ORAL REHABILITATION   43 ( 12 )   921 - 928   2016.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:WILEY-BLACKWELL  

    This study aimed to examine hyaluronan (HA) metabolism in relation to the onset and progression of temporomandibular joint osteoarthritis (TMJ-OA) induced by mechanical overloading. Two-month-old and 6-month-old C57BL/6N mice were divided into experimental and untreated control groups (n = 5/group). A sliding plate was attached to the maxillary incisors of the experimental mice for 10 days to overload the condylar cartilage in TMJ. In experimental group, profound cartilage degradation was detected in haematoxylin-eosin, Safranin-O-Fast Green-stained sections. It was also shown that the cartilage degradation was greater in older mice in both the control and the experimental groups. The number of HABP-positive cells was decreased by mechanical overloading and with age. The reduction of HA expression was correlated with the progression of cartilage degradation induced by mechanical overloading. The absolute quantification of the mRNA expression related to HA synthesis and HA degradation was also performed in each group. The mRNA expression levels of HA synthase (HAS) 2 and 3 were lower in the experimental group compared with the control group in the younger mice. In contrast, the mRNA expression levels of the HA degradation gene, HYAL2 and KIAA1199, were higher in the experimental group compared with the control group in the older mice. Thus, mechanical overload differently affected the balance of HA degradation and HA synthesis in the older and younger mice, respectively. In conclusion, mechanical overloading affects HA metabolism and it might initiate or amplify the condylar cartilage degradation.

    DOI: 10.1111/joor.12443

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  • The Nuclear Receptor AhR Controls Bone Homeostasis by Regulating Osteoclast Differentiation via the RANK/c-Fos Signaling Axis Reviewed

    Takashi Izawa, Rieko Arakaki, Hiroki Mori, Takaaki Tsunematsu, Yasusei Kudo, Eiji Tanaka, Naozumi Ishimaru

    JOURNAL OF IMMUNOLOGY   197 ( 12 )   4639 - 4650   2016.12

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    The aryl hydrocarbon receptor (AhR) pathway plays a key role in receptor activator of NF-kappa B ligand (RANKL)-mediated osteoclastogenesis. However, the mechanism underlying the regulation of AhR expression in osteoclasts and the signaling pathway through which AhR controls osteoclastogenesis remain unclear. We found that the expression of AhR in bone marrow-derived osteoclasts was upregulated by RANKL at an earlier stage than was the expression of signature osteoclast genes such as those encoding cathepsin K and NFAT, cytoplasmic, calcineurin-dependent 1. In response to RANKL, bone marrow macrophages isolated from AhR(-/-) mice exhibited impaired phosphorylation of Akt and MAPK as well as NF-kappa B, whereas their response to M-CSF remained unchanged. Osteoclast differentiation mediated by the AhR signaling pathway was also regulated in an RANKL/c-Fos-dependent manner. Furthermore, ligand activation of AhR by the smoke toxin benzo[a] pyrene accelerated osteoclast differentiation in a receptor-dependent manner, and AhR-dependent regulation of mitochondrial biogenesis in osteoclasts was observed. Moreover, AhR(-/-) mice exhibited impaired bone healing with delayed endochondral ossification. Taken together, the present results suggest that the RANKL/AhR/c-Fos signaling axis plays a critical role in osteoclastogenesis, thereby identifying the potential of AhR in treating pathological, inflammatory, or metabolic disorders of the bone.

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  • H Amelotin gene expression is temporarily being upregulated at the initiation of apoptosis induced by TGF beta 1 in mouse gingival epithelial cells Reviewed

    Yohei Nakayama, Sari Matsui, Keisuke Noda, Mizuho Yamazaki, Yasunobu Iwai, Hiroyoshi Matsumura, Takashi Izawa, Eiji Tanaka, Bernhard Ganss, Yorimasa Ogata

    APOPTOSIS   21 ( 10 )   1057 - 1070   2016.10

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    Amelotin (AMTN) is expressed and secreted by ameloblasts in the maturation stage of amelogenesis and persist with low levels in the junctional epithelium (JE) of erupted teeth. The purpose of this study is to investigate the transcriptional regulation of the AMTN gene by transforming growth factor beta1 (TGF beta 1) in gingival epithelial (GE1) cells in the apoptosis phase. Apoptosis was evaluated by the fragmentation of chromosomal DNA and TUNEL staining. A real-time PCR was carried out to examine the AMTN mRNA levels induced by TGF beta 1 and Smad3 overexpression. Transient transfection analyses were completed using the various lengths of mouse AMTN gene promoter constructs with or without TGF beta 1. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the Smad3 bindings to the AMTN gene promoter by TGF beta 1. TGF beta 1-induced apoptosis in GE1 cells were detected at 24 and 48 h by DNA fragmentation and TUNEL staining. AMTN mRNA levels increased at 6 h and reached maximum at 24 h in GE1 cells. Luciferase activities of the mouse AMTN gene promoter constructs were induced by TGF beta 1. The results of the ChIP assays showed that there was an increase in Smad3 binding to Smad-binding element (SBE)#1 and SBE#2 after stimulation by TGF beta 1. Immunohistochemical localization of AMTN was detected in the JE, and the AMTN protein levels in Smad3-deficient mice were decreased compared with wild-type mice. AMTN mRNA levels were induced at the initiation of apoptosis by TGF beta 1, which mediated through the Smad3 bindings to SBEs in the mouse AMTN gene promoter.

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  • Rebamipide Attenuates Mandibular Condylar Degeneration in a Murine Model of TMJ-OA by Mediating a Chondroprotective Effect and by Downregulating RANKL-Mediated Osteoclastogenesis (vol 11, e0154107, 2016) Reviewed

    Takashi Izawa, Hiroki Mori, Takehiro Shinohara, Akiko Mino-Oka, Islamy Rahma Hutami, Akihiko Iwasa, Eiji Tanaka

    PLOS ONE   11 ( 8 )   e0162032   2016.8

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  • Rebamipide Attenuates Mandibular Condylar Degeneration in a Murine Model of TMJ-OA by Mediating a Chondroprotective Effect and by Downregulating RANKL-Mediated Osteoclastogenesis Reviewed

    Takashi Izawa, Hiroki Mori, Tekehiro Shinohara, Akiko Mino-Oka, Islamy Rahma Hutami, Akihiko Iwasa, Eiji Tanaka

    PLOS ONE   11 ( 4 )   e0154107   2016.4

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    Temporomandibular joint osteoarthritis (TMJ-OA) is characterized by progressive degradation of cartilage and changes in subchondral bone. It is also one of the most serious subgroups of temporomandibular disorders. Rebamipide is a gastroprotective agent that is currently used for the treatment of gastritis and gastric ulcers. It scavenges reactive oxygen radicals and has exhibited anti-inflammatory potential. The aim of this study was to investigate the impact of rebamipide both in vivo and in vitro on the development of cartilage degeneration and osteoclast activity in an experimental murine model of TMJ-OA, and to explore its mode of action. Oral administration of rebamipide (0.6 mg/kg and 6 mg/kg) was initiated 24 h after TMJ-OA was induced, and was maintained daily for four weeks. Rebamipide treatment was found to attenuate cartilage degeneration, to reduce the number of apoptotic cells, and to decrease the expression levels of matrix metalloproteinase-13 (MMP-13) and inducible nitric oxide synthase (iNOS) in TMJ-OA cartilage in a dose-dependent manner. Rebamipide also suppressed the activation of transcription factors (e.g., NF-kappa B, NFATc1) and mitogen-activated protein kinases (MAPK) by receptor activator of nuclear factor kappa-B ligand (RANKL) to inhibit the differentiation of osteoclastic precursors, and disrupted the formation of actin rings in mature osteoclasts. Together, these results demonstrate the inhibitory effects of rebamipide on cartilage degradation in experimentally induced TMJ-OA. Furthermore, suppression of oxidative damage, restoration of extracellular matrix homeostasis of articular chondrocytes, and reduced subchondral bone loss as a result of blocked osteoclast activation suggest that rebamipide is a potential therapeutic strategy for TMJ-OA.

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  • Smad3 Deficiency Leads to Mandibular Condyle Degradation via the Sphingosine 1-Phosphate (S1P)/S1P(3) Signaling Axis Reviewed

    Hiroki Mori, Takashi Izawa, Eiji Tanaka

    AMERICAN JOURNAL OF PATHOLOGY   185 ( 10 )   2742 - 2756   2015.10

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    Temporomandibular joint osteoarthritis is a degenerative disease that is characterized by permanent cartilage destruction. Transforming growth factor (TGF)-beta is one of the most abundant cytokines in the bone matrix and is shown to regulate the migration of osteoprogenitor cells. It is hypothesized that TGF-beta/Smad3 signaling affects cartilage homeostasis by influencing sphingosine 1-phosphate (S1P)/S1P receptor signaling and chondrocyte migration. We therefore investigated the molecular mechanisms by which crosstalk may occur between TGF-beta/Smad3 and S1P/S1P receptor signaling to maintain condylar cartilage and to prevent temporomandibular joint osteoarthritis. Abnormalities in the condylar subchondral bone, including dynamic changes in bone mineral density and microstructure, were observed in Smad3(-/-) mice by microcomputed tomography. Cell-free regions and proteoglycan Loss characterized the cartilage degradation present, and increased numbers of apoptotic chondrocytes and matrix metalloproteinase 13 chondrocytes were also detected. Furthermore, expression of SIP receptor 3 (S1P(3)), but not S1P(1) or S1P(2), was significantly down-regulated in the condylar cartilage of Smad3(-/-) mice. By using RNA interference technology and pharmacologic tools, S1P was found to transactivate Smad3 in an S1P(3)/TGF-beta type II receptor-dependent manner, and S1P(3) was found to be required for TGF-beta-induced migration of chondrocyte cells and downstream signal transduction via Rac1, RhoA, and Cdc42. Taken together, these results indicate that the Smad3/S1P(3) signaling pathway plays an important role in the pathogenesis of temporomandibular joint osteoarthritis.

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  • An orthodontic case of skeletal Class III malocclusion with internal derangement of temporomandibular joint Reviewed

    Shinahara Takehiro, Watanabe Keiichiro, Mori Hiroki, Izawa Takashi

    The JOURNAL OF CHU-SHIKOKU ORTHODONTIC SOCIETY   27 ( 1 )   39 - 48   2015.8

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  • ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis Reviewed

    Takashi Izawa, Nidhi Rohatgi, Tomohiro Fukunaga, Qun-Tian Wang, Matthew J. Silva, Michael J. Gardner, Michael L. McDaniel, Nada A. Abumrad, Clay F. Semenkovich, Steven L. Teitelbaum, Wei Zou

    CELL REPORTS   11 ( 10 )   1625 - 1637   2015.6

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    ASXL2 is an ETP family protein that interacts with PPAR gamma. We find that ASXL2-/- mice are insulin resistant, lipodystrophic, and fail to respond to a high-fat diet. Consistent with genetic variation at the ASXL2 locus and human bone mineral density, ASXL2-/- mice are also severely osteopetrotic because of failed osteoclast differentiation attended by normal bone formation. ASXL2 regulates the osteoclast via two distinct signaling pathways. It induces osteoclast formation in a PPAR gamma/c-Fos-dependent manner and is required for RANK ligand-and thiazolidinedione-induced bone resorption independent of PGC-1 beta. ASXL2 also promotes osteoclast mitochondrial biogenesis in a process mediated by PGC-1 beta but independent of c-Fos. Thus, ASXL2 is a master regulator of skeletal, lipid, and glucose homeostasis.

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  • ASXL2-director of skeletal and metabolic homeostasis. Reviewed

    Research highlights by, David Holmes

    Nature Reviews Endocrinology   11 ( 8 )   445   2015.6

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    DOI: 10.1038/nrendo.2015.102

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  • Talin1 and Rap1 are Critical for Osteoclast Function. Reviewed

    Zou W, Izawa T, Zhu T, Chappel J, Otero K, Monkley SJ, Critchley DR, Petrich BG, Morozov A, Ginsberg MH, Teitelbaum SL

    Molecular and Cellular Biology   33 ( 4 )   830 - 44   2013.2

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  • Fas-Independent T-Cell Apoptosis by Dendritic Cells Controls Autoimmune Arthritis in MRL/lpr Mice Reviewed

    Takashi Izawa, Tomoyuki Kondo, Mie Kurosawa, Ritsuko Oura, Kazuma Matsumoto, Eiji Tanaka, Akiko Yamada, Rieko Arakaki, Yasusei Kudo, Yoshio Hayashi, Naozumi Ishimaru

    PLOS ONE   7 ( 12 )   e48798   2012.12

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    Background: Although autoimmunity in MRL/lpr mice occurs due to a defect in Fas-mediated cell death of T cells, the role of Fas-independent apoptosis in pathogenesis has rarely been investigated. We have recently reported that receptor activator of nuclear factor (NF)-kappa B ligand (RANKL)-activated dendritic cells (DCs) play a key role in the pathogenesis of rheumatoid arthritis (RA) in MRL/lpr mice. We here attempted to establish a new therapeutic strategy with RANKL-activated DCs in RA by controlling apoptosis of peripheral T cells. Repeated transfer of RANKL-activated DCs into MRL/lpr mice was tested to determine whether this had a therapeutic effect on autoimmunity.
    Methods and Finding: Cellular and molecular mechanisms of Fas-independent apoptosis of T cells induced by the DCs were investigated by in vitro and in vivo analyses. We demonstrated that repeated transfers of RANKL-activated DCs into MRL/lpr mice resulted in therapeutic effects on RA lesions and lymphoproliferation due to declines of CD4(+) T, B, and CD4(-)CD8(-) double negative (DN) T cells. We also found that the Fas-independent T-cell apoptosis was induced by a direct interaction between tumor necrosis factor (TNF)-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) on T cells and TRAIL on Fas-deficient DCs in MRL/lpr mice.
    Conclusion: These results strongly suggest that a novel Fas-independent apoptosis pathway in T cells maintains peripheral tolerance and thus controls autoimmunity in MRL/lpr mice.

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  • c-Src Links a RANK/alpha v beta 3 Integrin Complex to the Osteoclast Cytoskeleton Reviewed

    Takashi Izawa, Wei Zou, Jean C. Chappel, Jason W. Ashley, Xu Feng, Steven L. Teitelbaum

    MOLECULAR AND CELLULAR BIOLOGY   32 ( 14 )   2943 - 2953   2012.7

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    RANK ligand (RANKL), by mechanisms unknown, directly activates osteoclasts to resorb bone. Because c-Src is key to organizing the cell's cytoskeleton, we asked if the tyrosine kinase also mediates RANKL-stimulated osteoclast activity. RANKL induces c-Src to associate with RANK(369-373) in an alpha v beta 3-dependent manner. Furthermore, RANK(369-373) is the only one of six putative TRAF binding motifs sufficient to generate actin rings and activate the same cytoskeleton-organizing proteins as the integrin. While c-Src organizes the cell's cytoskeleton in response to the cytokine, it does not participate in RANKL-stimulated osteoclast formation. Attesting to their collaboration, alpha v beta 3 and activated RANK coprecipitate, but only in the presence of c-Src. c-Src binds activated RANK via its Src homology 2 (SH2) domain and alpha v beta 3 via its SH3 domain, suggesting the kinase links the two receptors. Supporting this hypothesis, deletion or inactivating point mutation of either the c-Src SH2 or SH3 domain obviates the RANK/alpha v beta 3 association. Thus, activated RANK prompts two distinct signaling pathways; one promotes osteoclast formation, and the other, in collaboration with c-Src-mediated linkage to alpha v beta 3, organizes the cell's cytoskeleton.

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  • A comprehensive treatment case of severe deep bite with oligodontia

    Matsumoto Kazuma, Izawa, Takashi

    The JOURNAL OF CHU-SHIKOKU ORTHODONTIC SOCIETY   22 ( 1 )   49 - 56   2010.8

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  • Biomechanical and biochemical characteristics of the mandibular condylar cartilage Reviewed

    S. Kuroda, K. Tanimoto, T. Izawa, S. Fujihara, J. H. Koolstra, E. Tanaka

    OSTEOARTHRITIS AND CARTILAGE   17 ( 11 )   1408 - 1415   2009.11

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    The human masticatory system consists of a mandible which is able to move with respect to the skull at its bilateral temporomandibular joint (TMJ) through contractions of the masticatory muscles. Like other synovial joints, the TMJ is loaded mechanically during function. The articular surface of the mandibular condyle is covered with cartilage that is composed mainly of collagen fibers and proteoglycans. This construction results in a viscoelastic response to loading and enables the cartilage to play an important role as a stress absorber during function. To understand its mechanical functions properly, and to assess its limitations, detailed information about the viscoelastic behavior of the mandibular condylar cartilage is required. The purpose of this paper is to review the fundamental concepts of the biomechanical behavior of the mandibular condylar cartilage. This review consists of four parts. Part 1 is a brief introduction of the structure and function of the mandibular condylar cartilage. In Part 2, the biochemical composition of the mandibular condylar cartilage is summarized. Part 3 explores the biomechanical properties of the mandibular condylar cartilage. Finally, Part 4 relates this behavior to the breakdown mechanism of the mandibular condylar cartilage which is associated with the progression of osteoarthritis in the TMJ. (C) 2009 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

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  • Analysis of gene expression profiles in human periodontal ligament cells under hypoxia: The protective effect of CC chemokine ligand 2 to oxygen shortage Reviewed

    Yukiko Kitase, Masahiko Yokozeki, Shinji Fujihara, Takashi Izawa, Shingo Kuroda, Kotaro Tanimoto, Keiji Moriyama, Eiji Tanaka

    ARCHIVES OF ORAL BIOLOGY   54 ( 7 )   618 - 624   2009.7

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    Periodontal ligament (PDL) cells appear to play important functional roles in response to mechanical stress. We hypothesized that hypoxia caused by a deformation of blood vessels and the following ischaemia may play a crucial role in differential gene expression in PDL cells affected by mechanical stress. Gene induction in cultured human PDL cells by hypoxia was analyzed using cDNA array, followed by RT-PCR analysis. Eleven hypoxia-responsive genes were found differentially expressed under low-oxygen conditions in PDL cells. Among them, CCR2, CC chemokine ligand 2 (CCL2) receptor was studied in more detail since little information is available on the role of chemokines in adaptive responses of PDL cells under hypoxia. Here we investigate whether CCR2 mediates the signalling to maintain the homeostasis of PDL cells. We found that cell death of PDL cells was induced under hypoxia with down-regulation of CCL2 mRNA expression. However, the exogenous CCL2 prevented PDL cell death under oxygen shortage with the increment of cellular inhibitor of apoptosis (cIAP) mRNA expression. The present study demonstrated substantial effects of hypoxia on gene expression of CCL2 and CCR2 in PDL cells, indicating that mechanical loading accompanied with mild hypoxia allows PDL cells to elicit adaptive responses with up-regulation of CCR2. (C) 2009 Elsevier Ltd. All rights reserved.

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  • Regional differences in fiber characteristics in the rat temporalis muscle Reviewed

    E. Tanaka, R. Sano, N. Kawai, J. A. M. Korfage, S. Nakamura, T. Izawa, G. E. J. Langenbach, K. Tanne

    JOURNAL OF ANATOMY   213 ( 6 )   743 - 748   2008.12

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    The behavioral differences in muscle use are related to the fiber type composition of the muscles among other variables. The aim of this study was to examine the degree of heterogeneity in the fiber type composition in the rat temporalis muscle. The temporalis muscle was taken from 10-week-old Wistar strain male rats (n = 5). Fiber types were classified by immunohistochemical staining according to their myosin heavy chain content. The anterior temporalis revealed an obvious regional difference of the fiber type distribution, whereas the posterior temporalis was homogeneous. The deep anterior temporalis showed a predominant proportion of type IIA fibers and was the only muscle portion displaying slow type fibers (&lt; 10%). The other two muscle portions, the superficial anterior and posterior temporalis, did not differ significantly from each other and contained mainly type IIB fibers. Moreover, the deep anterior temporalis was the only muscle portion showing slow type fibers (&lt; 10%). In the deep portion, type IIX fibers revealed the largest cross-sectional area (1943.1 +/- 613.7 mu m(2)), which was significantly (P &lt; 0.01) larger than those of type IIA and I + IIA fibers. The cross-sectional area of type IIB fibers was the largest in the remaining two muscle portions and was significantly (P &lt; 0.01) larger than that of type IIX fibers. In conclusion, temporalis muscle in rats showed an obvious heterogeneity of fiber type composition and fiber cross-sectional area, which suggests multiple functions of this muscle.

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  • A case report of condylar remodeling after orthognathic surgery with a combination of intraoral vertical ramus osteotomy and sagittal split ramus osteotomy Reviewed

    Takashi Izawa, Shinya Horiuchi, Keiko Tsuji, Shinji Fujihara, Yasuo Oba, Eiji Tanaka, Keiji Moriyama

    Journal of the Japanese Society for the Temporomandibular Joint   Vol.20 ( No.2 )   134 - 138   2008.8

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  • A case of spaced arch with enamel hypoplasia Reviewed

    Fujihara Shinji, Horiuchi Shinya, Izawa Takashi, Tsuji Keiko, Oba Yasuo, Moriyama Keiji

    The JOURNAL OF CHU-SHIKOKU ORTHODONTIC SOCIETY   20 ( 1 )   55 - 60   2008.8

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  • 下顎枝垂直骨切り術と下顎枝矢状分割術を併用した外科的矯正治療後に下顎頭のリモデリングを認めた一症例 Reviewed

    井澤 俊, 堀内信也, 森山啓司

    日本顎関節学会雑誌   20 ( 2 )   134 - 138   2008

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  • RANKLシグナルを介した関節炎モデルマウス樹状細胞の機能解析 Reviewed

    井澤 俊, 林 良夫, 森山 啓司

    日本矯正歯科学会大会プログラム・抄録集   66回   145 - 145   2007.9

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  • Immunoregulatory role of RANKL-stimulated dendritic cells on autoimmune arthritis in MRL/Ipr mice Reviewed

    T. Izawa, N. Ishimaru, K. Moriyama, Y. Hayashi

    JOURNAL OF BONE AND MINERAL RESEARCH   22   S270 - S270   2007.9

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  • Crosstalk between RANKL and Fas signaling in dendritic cells controls immune tolerance Reviewed

    Takashi Izawa, Naozurni Ishimaru, Keiji Moriyama, Masayuki Kohashi, Rieko Arakaki, Yoshio Hayashi

    BLOOD   110 ( 1 )   242 - 250   2007.7

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    Although receptor activator of nuclear factor (NF)-kappa B ligand (RANKL) signaling has been shown to prolong the survival of mature dendritic cells (DCs), the association of RANKL pathway with Fas-mediated apoptosis is obscure. Here, we found that bone marrow-derived DCs (BMDCs) from the Fas-deficient strain MRL/lpr mice, could survive much longer than normal DCs. The expressions of Bcl-x and Bcl-2 and the nuclear transport of NF-kappa B of RANKL-stimulated BMDCs from MRL/lpr mice were significantly upregulated. By contrast, Fas expression of BMDCs from normal C57BL/6 and MRL+/+ mice was increased by RANKL stimulation, and an enhanced DC apoptosis was found when stimulated with both RANKL and anti-Fas mAb, which was associated with activation of caspase-3 and caspase-9. Furthermore, the expression of FLIPL, an inhibitory molecule against Fas-mediated apoptosis, in normal DCs was significantly decreased by RANKL and anti-Fas mAb. Indeed, the adoptive transfer of RANKL-stimulated DCs resulted in rapid acceleration of autoimmunity in MRL/lpr recipients. These findings indicate that the crosstalk between RANKL and Fas signaling in DCs might control immune tolerance.

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  • 顎関節症の歯科矯正患者の臨床統計学的研究(Clinico-statistical study of orthodontic patients with temporomandibular joint disorders) Reviewed

    Tsuji Keiko, Satake Hidetaka, Fujihara Shinji, Izawa Takashi, Horiuchi Shinya, Moriyama Keiji

    日本顎関節学会雑誌   19 ( 1 )   82 - 82   2007.4

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  • 関節リウマチ〜基礎解析からの新知見 MRL/lprマウスにおける自己免疫性関節炎に対するRANKL刺激樹状細胞の免疫制御的役割(Immunoregulatory role of RANKL-stimulated dendritic cells on autoimmune arthritis in MRL/lpr mice) Reviewed

    Izawa Takashi, Ishimaru Naozumi, Arakaki Rieko, Moriyama Keiji, Hayashi Yoshio

    日本免疫学会総会・学術集会記録   36   284 - 284   2006.11

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  • 関節炎モデルマウスを用いた樹状細胞移入による関節リウマチ病態の修飾 Reviewed

    大嶋 淳, 井澤 俊, 石丸 直澄, 林 良夫, 森山 啓司

    日本矯正歯科学会大会プログラム・抄録集   65回   217 - 217   2006.9

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  • 関節円板前方転位を有する顎関節症患者の顎顔面形態の特徴について Reviewed

    辻 けい子, 井澤 俊, 細木 秀彦, 前田 直樹, 佐竹 秀太, 堀内 信也, 森山 啓司

    日本顎関節学会雑誌   18 ( 1 )   83 - 83   2006.4

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  • RANKL刺激活性化DCを介したMRL/lprマウス関節炎の病態修飾 Reviewed

    井澤 俊, 石丸 直澄, 表原 文江, 新垣 理恵子, 大嶋 淳, 森山 啓司, 林 良夫

    日本免疫学会総会・学術集会記録   35   249 - 249   2005.11

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  • 関節リウマチ自然発症モデルマウスを用いた関節骨破壊機構の解析 Reviewed

    井澤 俊, 林 良夫, 森山 啓司

    日本口腔科学会雑誌   54 ( 4 )   495 - 496   2005.9

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  • Comparison of treatment changes produced by the bite jumping appliance and elastic open activator Reviewed

    Takashi Izawa, Keiko Tsuji, Ritsu Yamauchi, Shinya Horiuchi, Keiji Moriyama

    The JOURNAL OF CHU-SHIKOKU ORTHODONTIC SOCIETY   17 ( 1 )   15 - 23   2005.8

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  • 関節リウマチ自然発症モデルマウスを用いた関節骨破壊機構の解析 Reviewed

    井澤 俊, 大嶋 淳, 森山 啓司

    日本顎関節学会雑誌   17 ( 1 )   57 - 57   2005.4

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  • 下垂体腫瘍に伴う反対咬合2症例の矯正治療(Two orthodontic treatment cases of reversed occlusion associated with the pituitary tumor) Reviewed

    Yasue Akihiro, Horiuchi Shinya, Izawa Takashi, Oba Yasuo, Moriyama Keiji

    日本矯正歯科学会大会プログラム・抄録集   63回   101 - 101   2004.11

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  • 上顎前突症患者におけるbite jumping applianceとelastic open activatorの治療効果に関する検討 Reviewed

    井澤 俊, 辻 けい子, 山内 里津, 堀内 信也, 森山 啓司

    日本矯正歯科学会大会プログラム・抄録集   63回   247 - 247   2004.11

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  • Estrogen deficiency accelerates murine autoimmune arthritis associated with receptor activator of nuclear Factor-kappa B ligand-mediated osteoclastogenesis Reviewed

    T Yoneda, N Ishimaru, R Arakaki, M Kobayashi, T Izawa, K Moriyama, Y Hayashi

    ENDOCRINOLOGY   145 ( 5 )   2384 - 2391   2004.5

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    The aims of this study were to evaluate the in vivo effects of estrogen deficiency in MRL/lpr mice as a model for rheumatoid arthritis and to analyze the possible relationship between immune dysregulation and receptor activator of nuclear factor-kappaB ligand (RANKL)-mediated osteoclastogenesis. Experimental studies were performed in ovariectomized (Ovx)-MRL/lpr, Ovx-MRL +/+, sham-operated-MRL/ lpr, and sham-operated- MRL +/+ mice. Severe autoimmune arthritis developed in younger Ovx-MRL/lpr mice until 24 wk of age, whereas these lesions were entirely recovered by pharmacological levels of estrogen administration. A significant elevation in serum rheumatoid factor, anti-double-stranded DNA, and anti-type II collagen was found in Ovx-MRL/lpr mice and recovered in mice that underwent estrogen administration. A high proportion of CD4(+) T cells bearing RANKL was found, and an enhanced expression of RANKL mRNA and an impaired osteoprotegerin mRNA was detected in the synovium. An increase in both osteoclast formation and bone resorption pits was found. These results indicate that estrogen deficiency may play a crucial role in acceleration of autoimmune arthritis associated with RANKL-mediated osteoclastogenesis in a murine model for rheumatoid arthritis.

    DOI: 10.1210/en.2003-1536

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  • RANKL刺激樹状細胞移入によるMRL/lprマウス自己免疫性関節炎の病態修飾 Reviewed

    井澤 俊, 林 良夫, 森山 啓司

    日本矯正歯科学会大会プログラム・抄録集   62回   215 - 215   2003.10

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MISC

  • 内分泌撹乱物質AhRリガンドB[a]PはCyp1a1シグナルを介して破骨細胞分化および骨代謝を制御する Invited

    井澤俊, 吉川友理, 浜田勇作, 上岡寛

    第41回日本骨形態計測学会記録集 特別企画〜医用画像から新しい骨形態計測への橋渡しを担うAI〜   78 - 79   2022

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  • Analysis of molecular mechanism about epigenetic gene related to osteoclast differentiation and treatment strategy for osteoporosis

    IZAWA Takashi

    Sumitomo electronic group   15 - 20   2019.8

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  • Analysis of bone resorptive mechanism under osteoporosis via activated dioxin receptor by smoking.

    IZAWA Takashi

    Smoking Research Foundation Annual Research Report 2018 Endocrine and Metabolic Systems   489 - 493   2019.6

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  • Analysis of bone metabolism regulatory mechanism via AhR/RANKL signaling cross-talk. Invited

    IZAWA Takashi

    Research papers of the Suzuken Memorial Foundation   36   186 - 190   2019.2

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  • 低酸素応答遺伝子HIF−1alphaを標的とした創傷治癒促進ならびに瘢痕形成抑制法の開発 Invited

    IZAWA Takashi

    THE NAKATOMI FOUNDATION ANNUAL REPORT No. 29   2018.9

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  • Role of epigenetic gene ASXL on the osteoclast differentiation

    IZAWA Takashi

    Annual Report 2018 of The Mochida Memorial Foundation for Medical and Pharmaceutical Research Foundation   250 - 253   2018.8

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  • Analysis of bone resorptive mechanism under osteoporosis via activated dioxin receptor by smoking. Invited

    Takashi Izawa

    Smoking Research Foundation Annual Research Report 2017   441 - 445   2018.6

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  • 核内受容体AhRはRANK/c-Fosシグナル伝達経路を介して破骨細胞の分化を制御する

    井澤 俊, 新垣 理恵子, 田中 栄二, 石丸 直澄

    生命科学系学会合同年次大会   2017年度   [2P - 0943]   2017.12

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  • The nuclear receptor AhR controls bone homeostasis by regulating osteoclast differentiation via the RANK/c-Fos signaling axis

    Takashi Izawa, Eiji Tanaka, Naozumi Ishimaru

    JOURNAL OF BONE AND MINERAL RESEARCH   32   S346 - S346   2017.12

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  • 核内受容体AhRはRANK/c-Fosシグナル伝達経路を介して破骨細胞の分化を制御する

    井澤 俊, 田中 栄二, 石丸 直澄

    日本骨代謝学会学術集会プログラム抄録集   35回   203 - 203   2017.7

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  • ASXL2 Regulates Skeletal, Glucose and Lipid Homeostasis. Reviewed

    Nidhi Rohatgi, Takashi Izawa, Tomohiro Fukunaga, Qun-Tian Wang, Matthew Silva, Michael Gardner, Michael McDaniel, Clay Semenkovich, Wei Zou, Steven Teitelbaum

    JOURNAL OF BONE AND MINERAL RESEARCH   29   S69 - S69   2014.2

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  • アロマターゼ遺伝子欠損マウスにおけるシェーグレン症候群様病変と肥満との関連

    岩浅 亮彦, 石丸 直澄, 井澤 俊, 徳永 律子, 工藤 保誠, 田中 栄二

    日本矯正歯科学会大会プログラム・抄録集   72回   192 - 192   2013.10

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  • 関節リウマチモデルマウスにおける破骨細胞の機能亢進

    松本一真, 石丸直澄, 井澤俊, 日浅雅博, 大浦律子, 岩浅亮彦, 林良夫, 田中栄二

    日本矯正歯科学会大会プログラム・抄録集   70th   218 - 218   2011.10

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    J-GLOBAL

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  • 関節リウマチモデルマウスにおける破骨細胞の機能解析

    松本 一真, 石丸 直澄, 井澤 俊, 日浅 雅博, 田中 栄二, 林 良夫

    日本骨代謝学会学術集会プログラム抄録集   29回   256 - 256   2011.7

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  • RANKLとFasによる免疫応答の制御 Invited

    石丸直澄, 井澤 俊, 林 良夫

    臨床免疫・アレルギー科   55 ( 2 )   143 - 47   2011

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  • Crosstalk between RANKL and Fas signaling in dendritic cells controls immune tolerance Invited

    Clinical immunology & allergology   52 ( 5 )   471 - 77   2009

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    CiNii Article

    CiNii Books

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  • Role of dendritic cells stimulated with RANKL for modulation of autoimmune arthritis in MRL/lpr mice.

    T Izawa, K Moriyama, Y Hayashi

    JOURNAL OF BONE AND MINERAL RESEARCH   18   S396 - S396   2003.9

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  • RANKL刺激樹状細胞移入によるMRL/lprマウス自己免疫性関節炎の病態修飾

    井沢俊, 渡辺恵, 石丸直澄, 新垣理恵子, 寺井政憲, 小林大, 林良夫

    日本病理学会会誌   92 ( 1 )   223 - 223   2003.4

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  • シェーグレン症候群発症機構に関与するエストロゲン欠乏によるClassII発現調節の解析

    寺井政憲, 石丸直澄, 新垣理恵子, 渡辺恵, 井沢俊, 林良夫

    日本病理学会会誌   92 ( 1 )   204 - 204   2003.4

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  • Acceleration of autoimmune arthritis in MRL/lpr mice transferred with RANKL-stimulated dendritic cells.

    T Izawa, K Moriyama, Y Hayashi

    JOURNAL OF BONE AND MINERAL RESEARCH   17   S490 - S490   2002.9

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Presentations

  • Mechanistic analysis of palatal wound healing via aryl hydrocarbon receptor by smoking

    Takashi Izawa, Yusaku Hamada, Yuri Yoshikawa, Hiroshi Kamioka

    46th Japanese Cleft Palate Association  2022.5.26 

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    Event date: 2022.5.26 - 2022.5.27

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:Kagoshima  

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  • Analysis of bone resorptive mechanism focused on osteoclast differentiation via AhR-ligand B[a]P by cigarette smoke.

    Hiroko Takenaga, Takashi Izawa, Yuri Yoshikawa, Yusaku Hamada, Ziyi Wang, Hiroshi Kamioka

    The 80th Annual Meeting of Japanese Orthodontic Society  2021.11.5 

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    Event date: 2021.11.3 - 2021.11.5

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  • The AhR endogenous ligand FICZ regulates bone homeostasis by regulating osteoclast differentiation via AhR/Cyp1a1 signaling

    Yuri Yoshikawa, Takashi Izawa, Yusaku Hamada, Hiroko Takenaga, Ziyi Wang, Hiroshi Kamioka

    The 80th Annual Meeting of Japanese Orthodontic Society  2021.11.5 

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    Event date: 2021.11.3 - 2021.11.5

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  • The AhR ligand regulates bone homeostasis by regulating osteoclast differentiation via the AhR/Cyp1a1 signalling axis.

    Yuri Yoshikawa, Takashi Izawa, Yusaku Hamada, Hiroko Takenaga, Ziyi Wang, Hiroshi Kamioka

    The 39th Annual Meeting of the Japanese Society for Bone and Mineral Research  2021.10.9 

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    Event date: 2021.10.8 - 2021.10.10

    Language:English   Presentation type:Oral presentation (general)  

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  • The AhR ligand regulates bone homeostasis by regulating osteoclast differentiation via the AhR/Cyp1a1 signalling axis.

    Yuri Yoshikawa, Takashi Izawa, Yusaku Hamada, Hiroko Takenaga, Ziyi Wang, Hiroshi Kamioka

    The 41st annual meeting of Japanese society for bone morphometry  2021.7.3 

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    Event date: 2021.7.1 - 2021.7.3

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  • Bio-imaging analysis of osteoclastic bone destruction through RANKL/IGF signalling pathway by breast cancer metastasis Invited

    Takashi Izawa

    The 38th Annual Meeting of the Japanese Society for Bone and Mineral Research  2020.10.9 

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    Event date: 2020.10.9 - 2020.10.11

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

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  • Crosstalk between cytokine RANKL and AhR signaling in osteoclasts controls bone homeostasis

    Takashi Izawa, Yuri Yoshikawa, Naozumi Ishimaru, Hiroshi Kamioka

    The 9th International Orthodontic Congress (9th IOC)  2020.10.4 

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  • Immunoregulatory role of p21 on the development of osteoarthritis in the temporomandibular joint

    Khurel-Ochir T, Izawa T, Sakamaki T, Mori H, Iwasa A, Tanaka E

    2019.11 

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  • p21 deficiency is susceptible to TMJ-Osteoarthritis with mechanical stress

    Khurel-Ochir T, Izawa T, Sakamaki T, Mori H, Iwasa A, Tanaka E

    2019.10 

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  • p21 deficiency is susceptible to TMJ-Osteoarthritis with mechanical stress

    Khurel-Ochir T, Izawa T, Sakamaki T, Mori H, Iwasa A, Tanaka E

    American Society for Bone and Mineral Research 2019 Annual Meeting  2019.9 

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  • 内分泌撹乱物質AhRリガンドはCyp1a1シグナルを介して破骨細胞分化および骨代謝を制御する

    吉川友理, 井澤 俊, 上岡 寛

    第63回歯科基礎医学会学術大会 一般演題(ポスター発表)  2021.10.9 

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  • Nuclear receptor AhR regulates osteoclastogenesis through RANK/c-Fos signalling axis

    Journal of Japanese Society for Bone Morphometry  2020.6.19 

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  • Analysis of molecular pathogenesis in TMJ-OA via TGF-beta/Smad3 signaling Invited

    IZAWA Takashi

    The 32nd Annual Meeting of the Japanese Society for the Temporomandibular Joint, Symposium 1  2019.7.27  The Japanese Society for the Temporomandibular Joint

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    Venue:Tokyo  

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  • Analysis of bone metabolism regulatory mechanism via dioxin receptor AhR.

    IZAWA Takashi

    The 38th Annual Meeting of Japan Society for Molecular Pathology  2019.7.19 

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  • Analysis of bone metabolism regulatory mechanism via dioxin receptor AhR. Invited

    IZAWA Takashi

    NCGG seminar  2019.6.28  NCGG

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    Venue:Obu, Aichi  

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  • Bone regulatory mechanism via dioxin receptor AhR Invited

    IZAWA Takashi

    The 8th Tokushima Bone and Calcium seminar  2019.2.21 

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    Venue:Tokushima, Japan  

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  • S1P1/Fas signal crosstalk via NF-kB activation in osteoclasts controls subchondral bone remodeling in murine arthritis

    IZAWA Takashi

    The 47th Annual Meeting of The Japanese Society for Immunology  2018.12.10  The Japanese Society for Immunology

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    Venue:Hkata, Fukuoka, Japan  

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  • Fas-independent T-cell apoptosis by dendritic cells controls autoimmune arthritis in MRL/lpr mice

    IZAWA Takashi

    The 41st Annual Meeting of the Molecular Biology Society of Japan  2018.11.30  Molecular Biology Society of Japan

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    Venue:Yokohama, Japan  

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  • HIF-1α modulates the palatal wound healing via M1/M2 macrophage reprogramming

    Islamy Rahma Hutami, Takashi Izawa, a

    JADR 2018 -Back to the tangible -the symbiosis of basic research and clinical dentistry  2018.11.17  Japanese Association for Dental Research

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    Venue:Hkkaido University, Hokkaido, Japan  

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  • The role of p21 on the development of TMJ-OA

    Tsendsuren Khurel-Ochir, Takashi Izawa, Hiroki Mori, e, l, lenary, poster award

    The 77th Annual Meeting of the Japanese Orthodontic Society Academic Exhibits  2018.11.1  Japanese Orthodontic Society

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    Venue:Yokohama  

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  • Fas/S1P1 crosstalk via NF-kB activation in osteoclasts controls subchondral bone remodeling in murine TMJ arthritis International conference

    Islamy Rahma Hutami, Takashi Izawa

    ASBMR 2018 Annual Meeting  2018.9.29  American Society for Bone and Mineral Research

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    Venue:Montreal, Quebec, Canada  

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  • The nuclear receptor AhR controls bone homeostasis by regulating osteoclast differentiation via the RANK/c-Fos signaling axis.

    IZAWA Takashi

    The 60th Annual Meeting of Japanese Association for Oral Biology  2018.9.6 

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  • Fas-independent T-cell apoptosis by dendritic cells controls autoimmune arthritis in MRL/lpr mice

    Takashi Izawa, autho

    The 36th Annual Meeting of the Japanese Society for Bone and Mineral Research  2018.7.28  JSBMR

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    Venue:Nagasaki  

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  • HIF-1α regulates the palatal wound healing through M1/M2 macrophage reprogramming International conference

    Islamy Rahma Hutami, Takashi Izawa

    96th General Session & Exhibition of the IADR  2018.7.27  IADR Craniofacial Biology Research – Craniofacial Biology: Developmental Processes, Wound Healing and Tissue Regeneration

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    Venue:London Convention Center London, England  

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  • 喫煙によるダイオキシン受容体の活性化を介した骨粗症発症メカニズムの解明

    IZAWA Takashi

    第33回 平成29年度助成研究発表会 喫煙と内分泌・代謝  2018.7.24  Smoking Research Foundation

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    Venue:Keio Plaza Hotel, Tokyo  

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  • AhRはRANK/c-Fosシグナル伝達経路を介して破骨細胞の分化を制御する

    Takashi Izawa, autho

    The 4th Annual Meeting of Japanese Society of Osteoimmunology 2018 OKINAWA  2018.6.25 

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    Venue:OKINAWA  

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  • Signal crosstalk between cytokine RANKL and AhR signaling in osteoclasts controls bone homeostasis International conference

    Takashi Izawa, author, Rieko Arakaki, Naozumi Ishimaru

    IMMUNOLOGY 2018  2018.5.5  Annual Meeting of The American Association of Immunologists

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    Venue:Austin Convention Center Austin, TX, USA  

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  • Crosstalk between cytokine RANKL and AhR signaling in osteoclasts controls bone homeostasis International conference

    Takashi Izawa, author, Rieko Arakaki, Naozumi Ishimaru

    Gordon Research Conference; "Bones and Teeth" From Skeletal and Dental Stem Cells to Rare Bone Disease and Integrative Physiology  2018.1.30 

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    Venue:Houston TX, USA  

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  • Crosstalk between cytokine RANKL and AhR signaling in osteoclasts controls bone homeostasis International conference

    Takashi Izawa, author, Rieko Arakaki, Naozumi Ishimaru

    Gordon Research Seminar; "Bones and Teeth" Translating Mechanisms of Bone Formation and Repair  2018.1.28 

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    Venue:Houston, TX, USA  

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  • Crosstalk between cytokine RANKL and AhR signaling in osteoclasts controls bone homeostasis

    Takashi Izawa, Rieko Arakaki, Naozumi Ishimaru

    The 46th Annual Meeting of The Japanese Society for Immunology W16 Cytokines and chemokines-2  2017.12.12  Proceedings of the Japanese Society for Immunology

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    Venue:Sendai, Miyagi, Japan  

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  • The nuclear receptor AhR controls bone homeostasis by regulating osteoclast differentiation via the RANK/c-Fos signaling axis.

    Takashi Izawa, author, Rieko Arakaki, Naozumi Ishimaru

    ConBio2017  2017.12.7 

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  • 核内受容体AhRはRANK/c-Fosシグナル伝達経路を介して破骨細胞の分化を制御する

    Takashi Izawa

    2nd Skeletal Science Retreat  2017.11  JSBMR

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    Venue:Kurashiki  

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  • Role of hypoxia inducible factor-1 alpha in the palatal wound healing

    Islamy Rahma Hutami, Takashi Izawa, author) et al. plenary, poster award

    The 76th Annual Meeting of the Japanese Orthodontic Society Academic Exhibits  2017.10  Japanese Orthodontic Society

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    Venue:Sapporo, Hokkaido  

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  • The nuclear receptor AhR controls bone homeostasis by regulating osteoclast differentiation via the RANK/c-Fos signaling axis. International conference

    Takashi Izawa, autho

    ASBMR 2017 Annual Meeting  2017.9.11  American Society for Bone and Mineral Research

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    Venue:Denver, CO, USA  

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  • 核内受容体AhRはRANK/c-Fosシグナル伝達経路を介して破骨細胞の分化を制御する

    Takashi Izawa, autho, Naozumi Ishimaru

    The 35th Annual Meeting of the Japanese Society for Bone and Mineral Research  2017.7.29  JSBMR

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    Venue:Hakata, Fukuoka  

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  • Effect of Rebamipide administration on TMJ-OA model mouse International conference

    Hiroki Mori, Takashi Izawa, author) et

    95th General & Exihibition IADR 2017  2017.3  IADR

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    Venue:San Francisco, USA  

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  • Fas/S1P1 signaling controls temporomandibular joint subchondral bone remodeling in autoimmune-arthritis International conference

    Islamy Rahma Hutami, Takashi Izawa, author) et al. plenary, poster award

    95th General & Exihibition IADR 2017  2017.3  IADR

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    Venue:San Francisco, USA  

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  • The role of osteoclast in the spontaneously developed temporomandibular joint arthritis of the MRL/lpr mice.

    Islamy Rahma Hutami, Takashi Izawa, author)plenary poster award

    The 75th Annual Meeting of the Japanese Orthodontic Society Academic Exhibits  2016.11  Japanese Orthodontic Society

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    Venue:Tokushima, Japan  

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  • Rebamipide Attenuates Mandibular Condylar Degeneration in a Murine Model of TMJ-OA by Mediating a Chondroprotective Effect and by Downregulating RANKL-mediated Osteoclastogenesis.

    Takashi Izawa, autho

    13th Meeting of Bone Biology Forum  2016.8 

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    Venue:Makuhari  

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  • S1P/Smad3シグナルを介した顎関節における変形性関節症の病態解明

    Takashi Izawa

    第7回 骨バイオサイエンス研究会  2016.6 

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    Venue:Okayama  

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  • Role of Rho-GTP/S1P/Smad3 Signaling on the Pathogenesis of TMJ-OA International conference

    Hiroki Mori, Takashi Izawa, author) et

    International Association for Dental Research General Session  2016.6  IADR

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    Venue:Seoul  

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  • Smad3 deficiency leads to mandibular condyle degeneration via the Sphingosine 1-phosphate (S1P)/S1P3 signaling axis International conference

    Hiroki Mori, Takashi Izawa, author) et

    ASBMR 2015 Annual Meeting  2015.10  American Society for Bone and Mineral Research

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    Venue:Seattle, USA  

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  • ASXL2 Regulates Skeletal, Glucose and Lipid Homeostasis International conference

    Nidhi Rohatgi, Takashi Izawa, Tomohiro Fukunaga, Qun-Tian Wang, Matthew Silva, Micheal Gardner, Micheal McDaniel, Clay Semenkovich, Wei Zou, Steven Teitelbaum

    ASBMR 2014 Annual Meeting  2014.9  American Society for Bone and Mineral Research

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    Venue:Houston, TX, USA  

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  • RANK/integrin avb3/c-Src complex controls osteoclast cytoskeleton

    Izawa Takashi

    The 11th Oral Science Frontier  2013.3.2 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:Miyazaki, Japan  

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  • c-Src Links a RANK/alpha v beta 3 integrin Complex to the Osteoclast Cytoskeleton International conference

    Takashi Izawa, Wei Zou, Jean Chappel, Xu Feng, Steven Teitelbaum

    ASBMR 2012 Annual Meeting  2012.10  American Society for Bone and Mineral Research

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    Venue:Minneapolis, USA  

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  • Talin1 and Rap1 are Critical for Osteoclast Function International conference

    Wei Zou, Tingting Zhu, Takashi Izawa, Jean Chappel, Susan Monkley, David Critchley, Brian Petrich, Alexei Morozov, Mark Ginsberg, Steven Teitelbaum

    ASBMR 2012 Annual Meeting  2012.10  American Society for Bone and Mineral Research

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:Minneapolis, USA  

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  • c-Src Links a RANK/alpha v beta 3 integrin Complex to the Osteoclast Cytoskeleton International conference

    Takashi Izawa

    Avioli Musculoskeletal Seminar Series  2012.6  Washington University School of Medicine

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    Language:English   Presentation type:Oral presentation (keynote)  

    Venue:St. Louis, MO, USA  

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  • RANK regulates the Osteoclast Cytoskeleton in a c-Src/alpha v beta 3 Dependent Manner International conference

    Takashi Izawa, Wei Zou, Steven Teitelbaum

    ASBMR 2011 Annual Meeting  2011.9  American Society for Bone and Mineral Research

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    Venue:San Diego, CA, USA  

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  • Immunoregulatory role of RANKL-stimulated dendritic cells on autoimmune arthritis in MRL/lpr mice International conference

    Takashi Izawa, Naozumi Ishimaru, Keiji Moriyama, Yoshio Hayashi

    ACR/ARHP 71th Annual Scientific Meeting  2007.11  American College of Rheumatology

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    Venue:Boston, USA  

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  • Immunoregulatory role of RANKL-stimulated dendritic cells on autoimmune arthritis in MRL/lpr mice International conference

    Takashi Izawa, Naozumi Ishimaru, Keiji Moriyama, Yoshio Hayashi

    29th Annual Meeting of the American Society for Bone and Mineral Research  2007.9  American Society for Bone and Mineral Research

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    Venue:Honolulu  

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  • Role of dendritic cells stimulated with RANKL for modulation of autoimmune arthritis in MRL/lpr mice International conference

    Takashi Izawa, Keiji Moriyama, Yoshio Hayashi

    25th Annual Meeting of the American Society for Bone and Mineral Research  2003.9  American Society for Bone and Mineral Research

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    Venue:Minneapolis, USA  

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  • Acceleration of autoimmune arthritis in MRL/lpr mice transferred with RANKL-stimulated dendritic cells International conference

    Takashi Izawa, Keiji Moriyama, Yoshio Hayashi

    24th annual meeting of the American Society for Bone and Mineral Research  2002.9  American Society for Bone and Mineral Research

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    Venue:San Antonio, USA  

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Awards

  • Plenary poster award, the 80th annual meeting of JOS

    2021.11   Japanese Orthodontic Society (JOS)   The AhR endogenous ligand FICZ regulates bone homeostasis by regulating osteoclast differentiation via AhR/Cyp1a1 signaling

    Yuri Yoshikawa, Takashi Izawa, Yusaku Hamada, Hiroko Takenaga, Ziyi Wang, Hiroshi Kamioka

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  • Ryobi Memorial foundation

    2021.10   Ryobi Memorial foundation  

    Takashi Izawa

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  • ASBMR 2019 Travel Award

    2019.8   Japanese Society for Bone and Mineral Research  

    IZAWA Takashi

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  • Young Investigator Grant (Year 3)

    2019.4   Smoking Research Foundation  

    IZAWA Takashi

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  • Cancer related basic research

    2019.2   Tokushima University and Taiho Pharmaceutical company basic research promotion   Principal Investigator

    Takashi Izawa

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  • Poster competition research winner

    2019.2   ASCO, Assocation of Orthodontics (Singapore) Congress   : HIF1 alpha regulates the palatal wound healing via M1/M2 macrophage reprogramming

    Hutami Rahma Islamy, IZAWA Takashi(Research Instructor

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    Award type:Award from international society, conference, symposium, etc.  Country:Singapore

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  • The 77th JOS plenary poster award

    2018.11   Japanese Orthodontic Society  

    IZAWA Takashi

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  • Research Clusters of Tokushima University

    2018.8   Tokushima University   2018 selected cluster research grant (Principal Investigator)

    IZAWA Takashi

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  • 2018 JSBMR Rising Stars Grant

    2018.7   The Japanese Society for Bone and Mineral Research  

    Takashi Izawa

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    http://jsbmr.umin.jp/prize/

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  • Young Investigator Grant (Year 2)

    2018.4   Smoking Research Foundation  

    Takashi Izawa

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  • Takeda Science Foundation

    2017.11   Takeda Science Foundation  

    IZAWA Takashi

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  • The Mochida Memorial Foundation for Medical and Pharmaceutical Research

    2017.11  

    IZAWA Takashi

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  • Sumitomo electric group

    2017.11  

    IZAWA Takashi

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  • Mitsui Sumitomo Insurance Welfare Foundation

    2017.11  

    IZAWA Takashi

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  • 76th JOS plenary poster award (Academic exhibition)

    2017.10   Japanese Orthodontic Society  

    IZAWA Takashi

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  • Young Investigator Grant (Year 1/3)

    2017.7   Smoking Research Foundation  

    Takashi Izawa

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  • The Nakatomi Foundation

    2017.3  

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  • SUZUKEN MEMORIAL FOUNDATION

    2016.12  

    IZAWA Takashi

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  • The 75th JOS plenary poster award

    2016.11   Japanese Orthodontic Society  

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  • The Ichiro Kanehara Foundation for the Promotion of Medical Science & Medical Care

    2016.10   The Ichiro Kanehara Foundation for the Promotion of Medical Science & Medical Care  

    IZAWA Takashi

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    Award type:Award from publisher, newspaper, foundation, etc. 

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  • 2016 Plenary Research Award of Tokushima University School of Dentistry

    2016.8   Tokushima University School of Dentistry  

    Takashi Izawa

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  • 74th JOS plenary poster award (corresponding author)

    2015.11   Japanese Orthodontic Society  

    Takashi Izawa

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  • 73th JOS plenary poster award (corresponding author)

    2014.10   Japanese Orthodontic Society  

    Takashi Izawa

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  • 68th JOS plenary poster award (corresponding author)

    2009   Japanese Orthodontic Society  

    Takashi Izawa

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  • 67th JOS plenary poster award (first author, corresponding author)

    2008   Japanese Orthodontic Society  

    Takashi Izawa

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    Country:Japan

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  • ASBMR Young Investigator Travel Grant

    2007.11   American Society for Bone and Mineral Research  

    IZAWA Takashi

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Research Projects

  • Mechanism of epigenetic regulation about bone remodeling in the ortho gnathic congenital diseases

    Grant number:22H03297  2022.04 - 2026.03

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

    Takashi Izawa

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

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  • Analysis of dysregulated bone healing mechanisms via aryl hydrocarbon receptor by smoking and its regulation

    Grant number:2022G023  2022.04 - 2025.03

    公益財団法人 喫煙科学研究財団  一般研究(喫煙と内分泌・代謝)  一般研究

    研究代表者, 井澤 俊, 共同研究者, 上岡 寛, 早野 暁

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  • Analysis of bone destruction mechanisms via RANKL and AhR signal crosstalk in osteoclasts

    2021.10 - 2022.09

    Ryobi foundation  2021年度研究助成 

    Takashi Izawa

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  • 喫煙によるダイオキシン受容体を介した口腔組織修復の破綻メカニズム解明への挑戦

    Grant number:21K19602  2021.07 - 2024.03

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

    井澤 俊

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

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  • Bone and mineral regulatory mechanism in the osteoporosis and rheumatoid arthritis and its epigenetic analysis

    2018.08 - 2019.01

    Tokushima University  Research Clusters of Tokushima University 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

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  • Analysis of bone metastatic tumor and bone destruction via insulin binding protein using in vivo imaging

    2018.07 - 2019.10

    Japanese Society for Bone and Mineral Metabolism  The JSBMR Rising Stars Grant 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\500000 ( Direct expense: \500000 )

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  • Epigenetic analysis of new bone remodeling mechanism in the dentofacial region.

    Grant number:18H03011  2018.04 - 2022.03

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

    井澤 俊, 川邉 紀章, 早野 暁, 植田 紘貴, 松本 健志, 竹下 淳, 泰江 章博, 岩浅 亮彦, 森 浩喜, 常松 貴明

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    Authorship:Principal investigator 

    Grant amount:\17290000 ( Direct expense: \13300000 、 Indirect expense:\3990000 )

    これまでの申請者らの予備検討でマクロファージをRANKL刺激後にAsxl1の発現が急激に上昇するというデータを得ており、破骨細胞への分化・活性化の過程でAsxl1が極めて重要な役割を果たしていることが示唆されることよりRANKLシグナルとAsxl1との関係を詳細に解析する。一方で、Asxl1の発現がどのように調節されているのか、またその調節に関与する因子の本体についてもよく判っていない。さらに、Asxl1の直接のターゲットであるBaP1、Ezh2、あるいは核内ホルモンレセプターとの結合と破骨細胞分化に関する研究も実施した。その結果、Asxl1をノックダウンしたマクロファージではRANKL刺激により破骨細胞形成能の著しい亢進がみられ、また細胞内シグナル伝達においてリン酸化Akt、MAPキナーゼの一つであるリン酸化p38、NF-κBのサブユニットであるリン酸化p65、リン酸化IκBαの亢進を認めた。一方でBaP1をノックダウンしたマクロファージでは破骨細胞形成の著しい減少がみられ、NFATc1、Integrin β3、c-Src、Cathepsin Kなどの破骨細胞分化マーカー及びRANKLによるリン酸化Akt、リン酸化IκBα、リン酸化JNKの発現が著しく減弱していることが明らかとなった。破骨細胞形成には2つのサイトカインRANKL、M-CSFが必須であることが知られているがAsxl1、BaP1をノックダウンしたマクロファージではコントロールと比較してM-CSF刺激においては細胞内シグナル伝達に差がみられなかった。これらの結果よりAsxl1はブレーキ役、BaP1はアクセルとして分子複合体を形成しミエロイド系マクロファージから破骨細胞の分化に重要な役割を果たすことが示唆された。

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  • 顎顔面領域稀少性遺伝子疾患における骨代謝制御機構とその破綻のエピゲノム解析

    Grant number:18KK0464  2018.04 - 2022.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Fund for the Promotion of Joint International Research (Fostering Joint International Research (A))  Fund for the Promotion of Joint International Research (Fostering Joint International Research (A))

    井澤 俊

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    Authorship:Principal investigator 

    Grant amount:\15600000 ( Direct expense: \12000000 、 Indirect expense:\3600000 )

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  • Treatment strategy for osteoporosis and the mechanism of bone metabolism and osteoclast differentiation by analyzing the epigenetic regulatory genes

    2018.01 - 2018.09

    Sumitomo Denko Foundation  2017 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1100000 ( Direct expense: \1100000 )

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  • Exploitation for diagnosis, treatment, and prevention method on osteoporosis with high risk for care targeting on epigenetic molecules

    2017.12 - 2018.11

    Mitsui Sumitomo Insurance Welfare Foundation  2017 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1200000 ( Direct expense: \1200000 )

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  • Analysis of epigenetic molecules in the osteoclast differentiation and treatment strategy for osteoporosis

    2017.11 - 2020.05

    Takeda Science Foundation  2017 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct expense: \2000000 )

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  • Role of epigenetic molecules in osteoclast differentiation and treatment remedy for osteoporosis

    2017.11 - 2018.12

    The Mochida Memorial Foundation for Medical and Pharmaceutical Research  2017 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\3000000 ( Direct expense: \3000000 )

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  • Challenge to control the palatal scar formation and to analyze the regulatory mechanizm of metabolic reprogramming via hypoxia inducible genes

    Grant number:17K19758  2017.06 - 2019.03

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

    IZAWA Takashi

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    Grant amount:\6370000 ( Direct expense: \4900000 、 Indirect expense:\1470000 )

    The blood flow in the wound scar region is known to be decreased compared to the surrounding area of the wound closure. Wound healing is a well-orchestrated complex process leading to the repair of injured tissues. It is suggested that HIF-1α signaling is involved in wound healing by regulating inflammatory cytokines such as such as TNF-α, MIP-1α, and MCP-1. Here, we investigated the role of HIF-1α signaling on M1/M2-like macrophage expression of heterozygous HIF-1α-deficient (HIF-1α HET) mice palatal wound healing. Histological examination showed that palatal wound closure in HIF-1α HET mice was delayed by the decreased infiltration of M1/M2 macrophage markers in parallel with the diminished production of Col1a1, MCP-1, MIP-1α compared with WT mice. These results suggest that HIF-1α signaling may play an important role in the regulation of palatal wound healing and HIF-1α deficiency aggravate the infiltration of M1/M2 macrophage.

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  • Analysis of bone resorptive mechanism under osteoporosis via activated dioxin receptor by smoking

    2017.04 - 2020.03

    Smoking Research Foundation  Young Investigator Grant 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1500000 ( Direct expense: \1500000 )

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  • Acceleration of wound healing and repression of wound scar formation by targeting about hypoxia inducible gene HIF1-α

    2017.03 - 2018.03

    The Nakatomi Foundation  2017 

    Takashi Izawa

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    Grant amount:\1500000 ( Direct expense: \1500000 )

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  • Analysis of bone metabolism via signal crosstalk between AhR and RANKL

    2016.12 - 2017.12

    Suzuken Memorial Foundation  2016 (H28) 16-038 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct expense: \2000000 )

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  • Analysis of bone metabolism by dioxin receptor AhR

    2016.10 - 2017.09

    The Ichiro Kanehara Foundation  2016 (H28) 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\450000 ( Direct expense: \450000 )

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  • Challenge to analyze the regulatory mechanism of bone metabolism by dioxin receptor AhR

    Grant number:15K15757  2015.04 - 2017.03

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

    IZAWA Takashi

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    Grant amount:\3640000 ( Direct expense: \2800000 、 Indirect expense:\840000 )

    The mechanism underlying the regulation of AhR expression in osteoclasts and the signaling pathway through which AhR controls osteoclastogenesis remain unclear. We found that the expression of AhR in bone marrow-derived osteoclasts was upregulated by RANKL at an earlier stage. Osteoclast differentiation mediated by the AhR signaling pathway was also regulated in a RANKL/c-Fos-dependent manner. AhR controls osteoclast differentiation via c-Fos/NFATc1 and mitochondrial biogenesis through PGC-1β.

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  • Analysis of bone and cartilage destruction mechanism via RANKL/Fas signaling in rheumatoid arthritis

    Grant number:25713063  2013.04 - 2016.03

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

    IZAWA Takashi

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    Grant amount:\25350000 ( Direct expense: \19500000 、 Indirect expense:\5850000 )

    In this study, we investigated the functions of osteoclasts (OCs) from Fas-mutant MRL/lpr mice, murine model for rheumatoid arthritis (RA). In vitro and in vivo experiments showed hyperfunction of MRL/lpr OCs. Furthermore, the migratory response of MRL/lpr OC precursors to S1P was significantly enhanced. The hyper function of OCs in MRL/lpr mice play a potent role in the pathogenesis for RA with bone and cartilage destruction. Crosstalk between RANK/RANKL signaling and Fas/FasL signaling of OCs may regulate the differentiation and migratory function of OC precursors.

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  • Functional analysis of periostin -anti-apoptotic action of periostin in osteoblasts and periodontal ligament cells

    Grant number:20592404  2008 - 2010

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

    FUJIHARA Shinji, HORIUCHI Shinya, IZAWA Takashi

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

    In this study, we examined the effect of periostin on the function of osteoblasts and periodontal ligament cells, such as apoptosis and the associated signal pathway. In the result, it is revealed that periostin is associated with the apoptosis of periodontal ligament cells by the hypoxia-induced system, and the signaling pathway including FAK, JNK, ERK, P38 and AKT. Additionally, in the signaling pathway of β-catenin, periostin might affect the anti-apoptotic action in various cells.

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  • Regulation of bone and cartilage destruction via RANKL/Fassignaling crosstalk in temporomandibular joint.

    Grant number:20791579  2008 - 2009

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

    IZAWA Takashi

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    Grant amount:\4290000 ( Direct expense: \3300000 、 Indirect expense:\990000 )

    The aim of this study was to analyze the effect of dedritic cells (DCs) transfer stimulated with RANKL on the development. of murine autoimmune arthropathy. Three times of RANKL-stimulated DCs transfer into arthritis model mice increased the T cell apoptosis in vivo, and protected the development of autoimmune arthritis. These data indicate that RANKL pathway plays a crucial role for immunomodulation of murine autoimmune arthropathy.

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  • Molecular mechanism of TMJ-RA bone and cartilage destruction in the field of osteoimmunology

    2008 - 2009

    QOL (Univ. of Tokushima Young Investigator Research)  Category(Regulation of oral environment) 

    Takashi Izawa

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\700000 ( Direct expense: \700000 )

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  • Development of a novel zinc releasing cement by conversions of zinc phosphate into zinc calcium phosphate

    Grant number:19592355  2007 - 2009

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

    HORIUCHI SHINYA, TSUJI Keiko, IZAWA Takashi, FUJIHARA Shinji, TANAKA Eiji, KINOUCHI Nao

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

    Zinc releasing apatite cement was developed from zinc calcium phosphate derived from zinc phosphate, introduced into apatite cement. The proliferations of osteoblastic-cells and alkaline phosphatase activities were enhanced when the cells were cultured on this cement. It is suggested that this novel cement potent promotive effect as the bone cement.

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  • Analysis of cytoskeieton regulation system by Rho family protein RhoE in periodontal ligament cells

    Grant number:19592356  2007 - 2008

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

    KINOOUCHI Nao, FUJIHAR Shinji, SHIOYASONO Atsushi, KITASE Yukiko, TANAKA Eiji, IZAWA Takashi, TANIMOTO Yukiho

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    Authorship:Coinvestigator(s) 

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

    歯根膜は、歯槽骨に歯を植立する懸架組織であり、その主な構成要素はコラーゲンの太い束から成る歯根膜線維と線維芽細胞系の歯根膜細胞である。矯正力に伴う歯の移動において、歯根膜組織は圧縮や伸展といった形態変化を引き起こした後にリモデリングを行い、一定の形態を維持しながら歯根とともに歯槽骨内を移動する。歯根膜組織が介在しない骨癒着歯やインプラントでは歯周組織のリモデリングは起こらず歯は移動しないことからも、矯正歯科治療において歯根膜は極めて重要な組織であり、歯根膜の機械的刺激に応答したリモデリングや形態維持機構において、歯根膜細胞が中心的役割を演じていると考えられる。ところが、歯根膜細胞がどのような機構で機械的シグナルを生物学的シグナルに変換し、歯根膜組織のリモデリングや恒常性に関与しているのか、未だ詳細は不明である。過去に我々は、歯根膜細胞における力学的刺激応答性の分子制御機構を解明することを目的として、コラーゲンゲル中で三次元培養したヒト歯根膜細胞に圧縮力を負荷し、遺伝子発現パターンをマイクロアレイ法にて網羅的に解析した。その結果、圧縮力負荷群において低分子量GTP結合タンパクであるRh。ファミリーのRhoEが高発現していることを見出している(Araujo RMS, Oba Y, MoriyamaK : J PeriodontRe8, (42)15-22, 2007)。
    一方、Rhoファミリーは、アクチン細胞骨格の再編成を介して様々な細胞機能を制御することが知られており、なかでもユニークなRndサブファミリーに属するRh。E(Rnd3)も細胞骨格制御に関与すると考えられているが、歯根膜細胞においては全く報告を見ない。過去に、我々はRh。Eの細胞骨格制御における役割を検討したところ、圧縮力によりRhoEが発現上昇し、ストレスファイバー形成が抑制されたが、RhoEアンチセンスオリゴを導入するとストレスファイバー形成が回復したことから(Oba Y et.al, Orthodontic Waves2008)、RhoEは歯根膜細胞において細胞骨格形成に抑制的に作用することを見出し、RhoEが歯根膜再薄のストレスファイバー形成の制御に重要な役割を担っている可能性が示唆された。
    そこで、本研究では歯根膜細胞の機械的刺激に応答した細胞骨格リモデリングにおけるRhoEの役割を解明することを目的に、培養歯根膜細胞に圧縮力を加え、メカニカルストレス負荷時の歯根膜細胞の細胞骨格制御、とくにストレスファイバー(Fアクチン)形成におけるRhoEの役割をin vitroならびにin vivoにおいて以下の検討を行った。
    まず、RhoEの三次元的な細胞内局在の解析と細胞骨格制御における役割に関して、メカニカルストレスに応答して発現する歯根膜細胞のRhoEの細胞内局在を三次元的に詳細に調べ、RhoA、Rac、Cdc42などの発現を比較検討したところ、RhoEの発現が上昇することが確認された。また、RhoEの機能に関する検討に関して、メカニカルストレス負荷の歯根膜細胞において、アンチセンスやRhoEに特異的な合成二本鎖RNAを用いINAiにてRhoEの発現制御を行ったところ、ストレスファイバー形成がRhoEにて制御されることを確認した。さらに、加重負荷後1時間から48時間の各時間におけるストレスファイバー形成の観察にっいて検討したところ、ストレスファイバー形成がRhoEにて制御されることが確認できた。
    この結果を踏まえて、歯の移動時の歯根膜組織におけるRhoEの役割と、それに伴う歯根膜細胞の形態変化や細胞の分化制御をRhoEや細胞骨格関連因子の発現を検索し解析することを目的に、RhoEに対するin vivoでのRNAiを試みている。今回の実験では為害性が少なく, 近年マウス皮下腫瘍や全身性転移癌に対するsiRNA導入実験でその有効性が確認されているアテロコラーゲンを担体として用いsiRNAの導入を行っている。すなわち、RhoEに特異的な二本鎖RNA(siRNA)とアテロコラーゲンを最適な濃度比率で混合した後、lo週齢のc57BL/6マウスの歯周組織にin vivo投与しRNAiを行いその抑制効果を検討している最中である。
    以上のことから、RhoEが歯根膜細胞の細胞骨格制御に深く関わっている可能性は極めて高いと考えられ、力学的刺激に応答した歯根膜組織のリモデリング機序や細胞形態の維持機能はRhoEを介する歯根膜細胞の細胞機能制御が関与していることが示唆された。本研究を通じて、力学的刺激に伴う歯根膜細胞の分子制御機構の一端が明らかになれば、歯の移動における生物学的基礎的データとして歯科矯正学分野に大きく貢献するものと思われる。また、本研究は歯周治療やインプラント、さらには歯根膜再生医学の進歩にも大きく寄与すると考えられ、新しい歯科医療の開拓と治療戦略の構築に大きく貢献するものと期待される。

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  • Basic study for developing new therapies and its practical use for craniofacial anomalies

    Grant number:18209060  2006 - 2008

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

    MORIYAMA Keiji, OBA Yasuo, TAKAHASHI Takumi, KITASE Yukiko, TANIMOTO Yukiho, IZAWA Takashi, FUJIHARA Shinji, SUZUKI Shoichi, ONO TAKASHI, SUDA NAOTO, BABA Yoshiyuki, KAWAMOTO Tatsuo, TSUJI Michiko, HAMADA Takashi, OGAWA Takuya, SUZUKI Shoichi, ONO Takashi, BABA Yoshiyuki, KAWAMOTO Tatsuo, TSUJI Michiko

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    Authorship:Coinvestigator(s) 

    Grant amount:\49010000 ( Direct expense: \37700000 、 Indirect expense:\11310000 )

    頭蓋冠縫合部早期癒合症を主症状の1つとするApert症候群の原因として、FGFR 2の細胞外領域における2種類の変異(S252W、P253R)が報告されている。我々は、S252W型変異が骨芽細胞分化に及ぼす影響を検討することを目的として、S252W型変異体(FGFR2IIIc-S252W)と、その細胞外領域のみを含む可溶性変異体(soluble FGFR2 IIIc-S252W)を過剰発現させたトランスジェニックマウスを作出した。マウスの頭蓋冠由来の骨芽細胞を単離し、種々の解析を加えた結果、FGFR2IIIc-S252Wは骨芽細胞分化を亢進するのに対し、solubleFGFR2IIIc-S252Wはこのプロセスを抑制した。可溶性変異体による分化制御が、頭蓋冠縫合部早期癒合症に対する新規治療法に発展する可能性が期待される。

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  • RANKLシグナルを介した関節リウマチ顎関節破壊機構の解明

    Grant number:18791553  2006 - 2007

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

    井澤 俊

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    Authorship:Principal investigator 

    Grant amount:\3500000 ( Direct expense: \3500000 )

    関節リウマチ(Rheumatoid Arthritis : RA)の病態形成機構については不明な点が多い。本研究はRAの自然発症モデルとして知られているMRL/1prマウスの樹状細胞(Dendritic Cell : DC)の機能を詳細に解析し、RANKLシグナルを介したDCの活性化・維持機構を明らかにした上で、MRL/1prマウスにRANKL刺激により活性化したDCを移入することによる関節病変への影響について検討した。その結果、MRL/1prマウスの脾臓およびリンパ節においてMRL+/+マウスと比較してDCの細胞数の有意な増加が認められ、特にB220^-CD11_c^+CD8_a^+またはB220^-CD11_c^+CD11_b^+のMyeloid DCの割合が増加していた。一方、MRL/1prマウス由来のBone Marrow DCをRANKLで刺激すると活性化の亢進が見られ、抗アポトーシス分子(Bc1-2,Bc1-XL)の発現上昇、NF-κB活性の上昇が検出された。また正常DCをRANKLで刺激するとFasの発現、抗Fas抗体でのアポトーシスの亢進が認められた。さらに、RANKL刺激DCをMRL/1prマウスに移入すると骨破壊を伴ノうRA病変の増悪が観察された。したがって、MRL/1prマウスのRA病態形成にDCの機能異常が重要な役割を果たしていることに加え、RANKL及びFasの下流分子の中でNF-kBの活性化異常により最終的な樹状細胞の運命が決定されることを明らかにした(Blood 110:242-50,2007)。

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  • RNAiを用いた顎口腔系の骨格筋量制御法の開発に関する研究

    Grant number:17659648  2005 - 2006

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

    森山 啓司, 大庭 康雄, 井澤 俊, 金子 和之, 塩屋園 敦, 佐竹 秀太, 泰江 章博, 西 真寿美

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    Authorship:Coinvestigator(s) 

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

    咀嚼筋や舌筋の機能異常は、不正咬合の成因や矯正治療の予後の安定性に影響を与える。近年、細胞内の標的遺伝子の発現を特異的に抑制するRNA干渉法(RNA interference : RNAi)が開発され、臨床応用への展開が期待されている。本研究では、筋形成の新たな制御方法を開発することを目的として、骨格筋形成の抑制遺伝子であるマイオスタチン(Mst)を標的遺伝子としたRNAiがマウス筋芽細胞の増殖および分化に及ぼす影響を検討した。
    COS-1細胞で一過性に強制発現させたマイオスタチンはpSi-Mstをco-transfectionすることでその発現が顕著に抑制された。マイオスタチン恒常発現株では親株と比較して有意に細胞増殖能が低下していたが、pSi-Mstを導入すると細胞増殖能が有意に促進された。マイオスタチン恒常発現株における細胞増殖関連因子p21、p53およびpRbの発現に対するpSi-Mstの影響を検討した結果、p21、p53の発現上昇とpRbの発現低下が認められた。一方、pSi-Mstを導入したマイオスタチン恒常発現株では筋分化制御因子MyoD、myogeninおよびMHCの発現上昇と筋管形成を伴う筋分化促進が認められた。また、Mst-siRNAを混合したアテロコ・ラーゲンを導入したマウス咬筋において、導入から2週間後、対照群と比較してマイオスタチン発現が顕著に抑制されており、肉眼的にも明らかな骨格筋増大が観察された。Mst-siRNAを導入した咬筋および大腿二頭筋の重量は、いずれも有意な増加を示した。さらに、組織学的解析を行ったところ、Mst-siRNAを導入した咬筋の各筋線維は明らかな肥大傾向を示し、各筋線維の直径を測定・定量化した結果,対照群に比べて平均で約1.3倍増加していた。以上の結果から、マイオスタチンを標的としたRNAiは、筋芽細胞の増殖および分化を促進し、さらには個体レベルでの骨格筋量の調節に有用であり、今後骨格筋異常を伴う種々の疾患に対する非侵襲的かつ安全な治療として応用しうる可能性が示唆された。

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