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Cardiac developmental defects and eccentric right ventricular hypertrophy in cardiomyocyte focal adhesion kinase

Xu Peng1, Xiaoyang Wu, Joseph E Druso

  • 1Departments of Molecular Medicine, Clinical Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.

Proceedings of the National Academy of Sciences of the United States of America
|May 2, 2008
PubMed

Insights

Focal adhesion kinase (FAK) is crucial for embryonic heart development. Inactivating FAK in cardiomyocytes leads to cardiac defects and altered MEF2a expression, highlighting FAK

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Developmental Biology

Background:

  • Focal adhesion kinase (FAK) is a key mediator of integrin signaling.
  • FAK's role in embryonic cardiac development requires further elucidation.

Purpose of the Study:

  • To investigate the function and molecular mechanisms of FAK in embryonic cardiomyocyte development.
  • To determine the impact of FAK inactivation on cardiac structure and gene expression.

Main Methods:

  • Generation of conditional FAK knockout mice (CFKO-2a) using MLC2a-Cre.
  • Analysis of embryonic lethality, cardiac morphology, and cardiomyocyte proliferation.
  • Transmission electron microscopy and microarray analysis to assess cellular changes and gene expression.

Main Results:

  • Conditional FAK knockout resulted in embryonic lethality with thin ventricular walls and septal defects.
  • Surviving adult mice exhibited right ventricle hypertrophy and rough endoplasmic reticulum swelling.
  • FAK inactivation decreased cardiomyocyte proliferation and compromised myocyte enhancer factor 2a (MEF2a) expression, mediated by Src signaling.

Conclusions:

  • FAK is essential for embryonic cardiac development, regulating cardiomyocyte proliferation and MEF2a expression.
  • Src signaling downstream of FAK is critical for MEF2a regulation in the developing heart.

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