In vitro analyses of the pathogenesis of hypertrophic cardiomyopathy by using cardiomyocyte differentiation system
Project/Area Number |
21790985
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Pediatrics
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Research Institution | Osaka University |
Principal Investigator |
OKADA Yoko Osaka University, 大学院・医学系研究科, 寄附講座助教 (30457022)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
Keywords | 心筋症 / 心筋細胞 / 分化誘導 / 肥大シグナル / レオパルド症候群 |
Research Abstract |
The mechanisms of cardiac hypertrophy associated with LEOPARD syndrome were analyzed by using P19CL6 cells, which is a convenient cardiomyocyte differentiation model in vitro. The LEOPARD-type mutant SHP2 attenuated the terminal differentiation of cardiomyocyte with increased proliferative activity, as compared to the controls and Noonan-type SHP2 mutant. It also induced cardiomyocyte hypertrophy. These alterations were associated with the dysregulation of Akt/GSk3β/β-catenin pathway.
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Report
(3 results)
Research Products
(4 results)