Analysis of BMP-mediated cartilage formation anddifferentiation, and cartilage repair
| Project/Area Number |
21390421
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kyoto University (2011-2012)
Osaka University (2009-2010) |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥15,730,000 (Direct Cost: ¥12,100,000、Indirect Cost: ¥3,630,000)
Fiscal Year 2011: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2010: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2009: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
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| Keywords | 軟骨細胞 / 内軟骨性骨化 / ノックアウトマウス / 細胞分化 / HDAC4 / 軟骨 / 転写制御 / トランスジェニックマウス / コラーゲン |
|---|
| Research Abstract |
Sox9 in mesenchymal progenitors is important for their differentiation intochondrocytes, but its functions after differentiation into chondrocytes have not beendetermined. To investigate Sox9 function in chondrocytes precisely, we deleted Sox9genes after differentiation into chondrocytes in mice. Sox9 inactivation inchondrocytes resulted in apoptosis. Molecular analysis revealed that Sox9 sustainswhich are involved in chondrocyte differentiation, we discovered that chondrocytehypertrophy was markedly delayed in the growth plate cartilage in mice lacking saltinducible kinase 3 (SIK3). SIK3 was required for anchoring HDAC4 in the cytoplasm,thereby releasing MEF2C, a critical facilitator of chondrocyte hypertrophy, fromsuppression by HDAC4 in the nuclei. From these results, we concluded that SIK3facilitates chondrocyte hypertrophy during formation and maintenance of cartilage
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Report
(4 results)
Research Products
(30 results)
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[Journal Article] SIK3 is essential forchondrocyte hypertrophy during skeletaldevelopment in mice2012
Author(s)
Sasagawa,S.,Takemori,H.,Uebi,T.,Ikegami,D.,Hiramatsu,K.,Ikegawa,S.,Yoshikawa,H.and Tsumaki,N.
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Journal Title
Development
Volume: 139巻
Issue: 6
Pages: 1153-1163
DOI
Related Report
Peer Reviewed
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[Journal Article] Conditional deletionof Bmpr1ab in differentiatedosteoclasts increases osteoblastic boneformation,increasing volume ofremodeling bone in mice.2011
Author(s)
Okamoto,M.,Murai,J.,Imai,Y.,Ikegami,D.,Kamiya,N.,Kato,S.,Mishita,Y.,Yoshikawa,H.and Tsumaki,N
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Journal Title
J.BoneMiner.Res.
Volume: 26巻
Issue: 10
Pages: 2511-22
DOI
Related Report
Peer Reviewed
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[Journal Article] Essential mesenchymal role of smallGTPase Rac1 in interdigital programmedcell death during limb development.2009
Author(s)
Suzuki D, Yamada A, Amano T, YasuharaR, Kimura A, Sakahara M,Tsumaki N,Takeda S, Tamura M, Nakamura M, Wada N,Nohno T, Shiroishi T, Aiba A, KamijoR.
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Journal Title
Dev. Biol.
Volume: 335
Pages: 396-406
Related Report
Peer Reviewed
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[Journal Article] Essential mesenchymal role of small GTPase Rac1 in interdigital programmed cell death during limb development.2009
Author(s)
Suzuki D, Yamada A, Amano T, Yasuhara R, Kimura A, Sakahara M, Tsumaki N, Takeda S, Tamura M, Nakamura M, Wada N, Nohno T, Shiroishi T, Aiba A, Kamijo R.
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Journal Title
Dev.Biol. 335
Pages: 396-406
Related Report
Peer Reviewed
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