| Project/Area Number |
15K20014
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Saitama Medical University |
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Principal Investigator |
TSUKAMOTO SHO 埼玉医科大学, 医学部, 助手 (20707658)
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| Research Collaborator |
KATAGIRI TAKENOBU 埼玉医科大学, 医学部, 教授 (80245802)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨・軟骨代謝学 / 細胞内シグナル伝達 / 骨系統疾患 / シグナル伝達 |
|---|
| Outline of Final Research Achievements |
Smad4 is an essential co-activator for intracellular signaling of the TGF-β family. We examined a role of the TGF-β family in postnatal regulatory mechanisms of the locomotive tissues by establishing a tamoxifen-inducible Smad4 conditional knockout (Smad4 cKO) mice. Bone volume was increased in Smad4 cKO mice by an increase of bone formation. Hypertrophic zone in epiphyseal growth plate was expanded in Smad4 cKO mice. Treatment of primary chondrocytes cultured in vitro with TGF-β1 suppressed chondrogenic differentiation. Taken together, our findings suggest that Smad4-dependent intracellular signaling of the TGF-β family regulates differentiation and function of osteoblasts and chondrocytes in postnatal mice.
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