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Am J Physiol Cell Physiol 284: C457-C474, 2003. First published October 9, 2002; doi:10.1152/ajpcell.00380.2002
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Vol. 284, Issue 2, C457-C474, February 2003

Caveolin-1 null mice develop cardiac hypertrophy with hyperactivation of p42/44 MAP kinase in cardiac fibroblasts

Alex W. Cohen1,2, David S. Park1,2, Scott E. Woodman1,2, Terrence M. Williams1,2, Madhulika Chandra3, Jamshid Shirani3,4, Andrea Pereira de Souza5, Richard N. Kitsis3, Robert G. Russell4, Louis M. Weiss3,4, Baiyu Tang5, Linda A. Jelicks5, Stephen M. Factor3,4, Vitaliy Shtutin4, Herbert B. Tanowitz3,4, and Michael P. Lisanti1,2

1 Department of Molecular Pharmacology, Albert Einstein College of Medicine; 2 Division of Hormone-Dependent Tumor Biology, The Albert Einstein Cancer Center; 3 Divisions of Cardiology and Infectious Disease, Department of Medicine, Albert Einstein College of Medicine and The Montefiore Medical Center; and 4 Department of Pathology and 5 Department of Physiology & Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461

Recently, development of a caveolin-1-deficient (Cav-1 null) mouse model has allowed the detailed analysis of caveolin-1's function in the context of a whole animal. Interestingly, we now report that the hearts of Cav-1 null mice are markedly abnormal, despite the fact that caveolin-1 is not expressed in cardiac myocytes. However, caveolin-1 is abundantly expressed in the nonmyocytic cells of the heart, i.e., cardiac fibroblasts and endothelia. Quantitative imaging studies of Cav-1 null hearts demonstrate a significantly enlarged right ventricular cavity and a thickened left ventricular wall with decreased systolic function. Histological analysis reveals myocyte hypertrophy with interstitial/perivascular fibrosis. Because caveolin-1 is thought to act as a negative regulator of the p42/44 MAP kinase cascade, we performed Western blot analysis with phospho-specific antibodies that only recognize activated ERK1/2. As predicted, the p42/44 MAP kinase cascade is hyperactivated in Cav-1 null heart tissue (i.e., interstitial fibrotic lesions) and isolated cardiac fibroblasts. In addition, endothelial and inducible nitric oxide synthase levels are dramatically upregulated. Thus loss of caveolin-1 expression drives p42/44 MAP kinase activation and cardiac hypertrophy.

caveolae; cardiomyopathy; signal transduction; cardiac fibroblasts


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