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Circulation Research. 1998;82:773-778

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(Circulation Research. 1998;82:773-778.)
© 1998 American Heart Association, Inc.


Original Contributions

Hypertrophy, Pathology, and Molecular Markers of Cardiac Pathogenesis

Karen L. Vikstrom, Teri Bohlmeyer, Stephen M. Factor, , Leslie A. Leinwand

From the Department of Molecular, Cellular, and Developmental Biology (K.L.V., L.A.L.), University of Colorado, Boulder; the Department of Medicine (T.B.), University of Colorado Health Science Center, Denver; and the Department of Pathology (S.M.F.), Albert Einstein College of Medicine, Bronx, NY.

Correspondence to Leslie A. Leinwand, PhD, Professor and Chair, Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Campus Box 347, Boulder, CO 80309-0347. E-mail leinwand{at}stripe.colorado.edu

Abstract—Increased ventricular expression of several genes, including atrial natriuretic factor (ANF), has been documented in experimental models of cardiac hypertrophy. It remains to be clarified whether altered expression of these genes is a consistent marker of the hypertrophy itself or a marker of some parallel pathogenetic process. Using a transgenic mouse model of hypertrophic cardiomyopathy as a tool, we assessed the relationship between the amount of ventricular ANF gene expression and the degree of hypertrophy as well as the relationship between the cells expressing ANF and tissue pathology. We determined that hypertrophy is not always associated with increased ventricular expression of ANF and that cells expressing ANF are found in regions of tissue pathology. We propose that alteration in the ventricular expression of this gene is a sensitive indicator of cardiac pathogenesis and may result from a number of different stimuli that include, among others, abnormal tissue architecture and hemodynamic load.


Key Words: hypertrophy • gene expression • pathogenesis • atrial natriuretic factor




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