Pathological mechanism of osteoarthritis -analysis of molecules responsing to mechanical stress-
Project/Area Number |
18591636
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | Kagoshima University |
Principal Investigator |
IJIRI Kosei Kagoshima University, Graduate School of Medical and Dental Sciences, Associate Professor (00315417)
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Co-Investigator(Kenkyū-buntansha) |
KOMIYA Setsuro Kagoshima University, Graduate School of Medical and Dental Sciences, Professor (30178371)
ISHIDOU Yasuhiro Kagoshima University, Graduate School of Medical and Dental Sciences, Research Associate Professor (10300740)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,790,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
Keywords | osteoarthritis / GADD45beta / Hypertrophic chondrocyte / 軟骨細胞 / OA / GADD45b / マウス |
Research Abstract |
In the next step, the expression of GADD45beta was examined using immunohistochemistry of articular cartilage from human and animal samples. GADD45beta was especially highly expressed in cluster of early OA cartilage in human reticular cartilage. The hypertrophic chondrocyte were positive in OA animal model but not in normal animal. These findings suggested GADD45beta functions to support the mechanism of dedifferentitation of chondrocyte during the process of OA. To examine the mechanical function of GADD45beta in terms of phenotype of chondrocyte, luciferase assay and real time PCR were performed using chondrocyte cell line. Interestingly, type X collagen and MMP-13 gene expressions were increased by GADD45beta over-expression, but decreased by GADD45beta suppressing using siRNA. Additionally, type II collagen gene expression was decreased by by GADD45beta over-expression and increased by by GADD45beta suppressing. We also investigated apoptosis analysis using ATDC5 cells. GADD45beta clearly functioned anti-apoptotic way. This protein accelerates Type X collagen and MMP-13 gene expression and suppresses Type II collagen gene expression. GAdd45beta also noble function in terms of anti-apoptosis in chondrocyte in vitro. These results suggest the importance of GADD45beta function in OA to support the survival of chondrocytes during the process of OA, resulting in dedifferentiation from normal chondrocyte.
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Report
(3 results)
Research Products
(7 results)
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[Journal Article] Differential Expression of GADD45β in Normal and Osteoarthritic Cartilage Potential Role in Homeostasis of Articular Chondrocytes2008
Author(s)
Ijiri, K., Zerbini, L., Peng, H., Out, HH., Tsuchimochi, K., Otero, M., Dragomir, C., Walsh, N., Bierbaum, BE., Mattingly, D., Flandern, G., Komiya, S., Aigner, T., Libermann, TA., Goldring, MB
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Journal Title
Arthritis Rheum 58
Pages: 2075-2087
Description
「研究成果報告書概要(欧文)」より
Related Report
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[Journal Article] ESE-1 is a Potent Pepressor of Type II Collagen Gene (LOL2A1) Transcription in Human Chondrocytes2008
Author(s)
Peng, H., Tan, L., Osaki, M., Zhan, Y., Ijiri, K., Tsuchimochi, K., Otero, M., Wang, H., Choy, BK., Grail, FT., Gu, X., Libermann, TA., Oettgen, P., Goldring, MB
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Journal Title
J Cell Physiol 215
Pages: 562-573
Description
「研究成果報告書概要(欧文)」より
Related Report
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