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In vitro analyses of the pathogenesis of hypertrophic cardiomyopathy by using cardiomyocyte differentiation system

Research Project

Project/Area Number 21790985
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeSingle-year Grants
Research Field Pediatrics
Research InstitutionOsaka 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.

Report

(3 results)
  • 2010 Annual Research Report   Final Research Report ( PDF )
  • 2009 Annual Research Report
  • Research Products

    (4 results)

All 2011 2010

All Presentation (4 results)

  • [Presentation] LEOPARD type SHP2 mutant Q510E attenuates cardiomyocyte differentiation via aberrant β-catenin signaling and promotes cardiomyocyte hypertrophy by PI3K/Akt pathway2011

    • Author(s)
      Ishida H, Okada Y, Ichimori H, Narita J, Kogaki S, Ozono K
    • Organizer
      Keystone Symposia Mechanisms of Cardiac Growth, Death, and Regeneration 2011
    • Place of Presentation
      Keystone, Colorado, USA
    • Year and Date
      2011-02-23
    • Related Report
      2010 Annual Research Report
  • [Presentation] LEOPARD type SHP2 mutant Q510E attenuates cardiomyocyte differentitation via aberrant β-catenin signaling and promotes cardiomyocyte hypertrophy by PI3K/Akt pathway.2011

    • Author(s)
      Ishida H, Okada Y, Ichimori H, Narita J, Kogaki S, Ozono K
    • Organizer
      Keystone Synposia Mechanisms of Cardiac Growth, Death, and Regeneration 2011
    • Place of Presentation
      Keystone Colorado USA
    • Year and Date
      2011-02-06
    • Related Report
      2010 Final Research Report
  • [Presentation] 心筋細胞分化誘導システムを用いたLEOPARD症候群における肥大型心筋症発症機構の解明2010

    • Author(s)
      石田秀和, 岡田陽子, 市森裕章, 成田淳, 小垣滋豊, 大薗恵一
    • Organizer
      日本小児循環器学会2010
    • Place of Presentation
      東京
    • Related Report
      2010 Final Research Report
  • [Presentation] 心筋細胞分化誘導システムを用いたLEOPARD症候群における肥大型心筋症発症機構の解明2010

    • Author(s)
      石田秀和, 岡田陽子, 市森裕章, 成田淳, 小垣滋豊, 大薗恵一
    • Organizer
      日本小児循環器学会総会2010
    • Place of Presentation
      東京
    • Related Report
      2010 Annual Research Report

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Published: 2009-04-01   Modified: 2016-04-21  

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