| Project/Area Number |
23592221
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
MAEDA Shingo 鹿児島大学, 医歯(薬)学総合研究科, 准教授 (60353463)
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| Co-Investigator(Kenkyū-buntansha) |
KOMIYA Setsuro 鹿児島大学, 大学院医歯学総合研究科, 教授 (30178371)
ISHIDOU Yasuhiro 鹿児島大学, 大学院医歯学総合研究科, 教授 (10300740)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 変形性関節症 / TGF-β / BMP / SnoN / 軟骨細胞 / TGF-beta, Sweden / chondrocyte / 軟骨細胞分化 / TGF-beta |
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| Research Abstract |
Osteoarthritis (OA) suppresses activity of patients, which conditions often lead patients to death. Loss of TGF-beta signaling in mice promotes hypertrophic maturation of chondrocytes in articular cartilage, the phenotype of OA. Among the downstream molecules of TGF-beta signaling, we focused on SnoN to examine its roles in chondrocyte maturation and pathogenesis of OA. SnoN was not expressed in human normal articular cartilage or immature chondrocytes of mice, while it was detected in human OA cartilage as well as in matured mouse chondrocytes. During BMP-induced chondrogenesis in vitro, SnoN suppressed BMP signaling to inhibit the chondrocyte maturation. Gain-of-function of SnoN mimicked the effects of TGF-beta application, therefore, SnoN was suggested to be a novel molecular target in treatment or prevention of OA.
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