2016 Fiscal Year Final Research Report
Runx1 contributes to articular cartilage maintenance through enhancement of cartilage matrix production and suppression of hypertrophic differentiation
| Project/Area Number |
25713052
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Yano Fumiko 東京大学, 医学部附属病院, 助教 (80529040)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Keywords | Runx1 / ルブリシン |
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| Outline of Final Research Achievements |
We analysed OA development of Col2a1-Cre;Runx1fl/fl and Runx1fl/fl mice by surgical induction of joint instability, and expression of marker proteins in the articular cartilage by immunostainings. The cartilage degradation and the osteophyte formation of Col2a1-Cre;Runx1fl/fl the joints after 8 weeks was accelerated compared with the Runx1fl/fl littermate joints. To know the regulation of chondrocyte differentiation by Runx1, we analysed a function of downstream molecules and interaction with co-factors. Knockdown of Runx1 in articular chondrocytes increased hypertrophic markers, and decreased Bapx1 and chondrogenic markers. The similar results were observed in the Col2a1-Cre;Runx1fl/fl knee joint cartilage. Notably, suppression of hypertrophic markers by Runx1 was diminished by silencing of Bapx1 by siRNA. The present data suggest that Runx1 contributes to articular cartilage maintenance through suppression of hypertrophic differentiation via Bapx1 induction.
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| Free Research Field |
整形外科 関節軟骨
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