| Budget Amount *help |
¥24,570,000 (Direct Cost: ¥18,900,000、Indirect Cost: ¥5,670,000)
Fiscal Year 2015: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2014: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2013: ¥8,970,000 (Direct Cost: ¥6,900,000、Indirect Cost: ¥2,070,000)
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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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