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J. Biol. Chem., Vol. 278, Issue 31, 28930-28937, August 1, 2003
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¶ || **
From the
Department of Molecular Biology, The
University of Texas, Southwestern Medical Center at Dallas, Dallas, Texas
75390-9148 and ¶Myogen Inc., Westminster,
Colorado 80021
Postnatal cardiac myocytes respond to stress signals by hypertrophic growth and activation of a fetal gene program. Recently, we showed that class II histone deacetylases (HDACs) suppress cardiac hypertrophy, and mice lacking the class II HDAC, HDAC9, are sensitized to hypertrophic signals. To further define the roles of HDACs in cardiac hypertrophy, we analyzed the effects of HDAC inhibitors on the responsiveness of primary cardiomyocytes to hypertrophic agonists. Paradoxically, HDAC inhibitors imposed a dose-dependent blockade to hypertrophy and fetal gene activation. We conclude that distinct HDACs play positive or negative roles in the control of cardiomyocyte hypertrophy. HDAC inhibitors are currently being tested in clinical trials as anti-cancer agents. Our results suggest that these inhibitors may also hold promising clinical value as therapeutics for cardiac hypertrophy and heart failure.
Received for publication, March 26, 2003 , and in revised form, May 12, 2003.
* This work was supported by grants from the National Institutes of Health, The Donald W. Reynolds Cardiovascular Clinical Research Center (Dallas, TX), The Texas Advanced Technology Program, and The William G. McGowan Charitable Fund, Inc. (to E. N. O.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Both authors contributed equally to this work.
|| A Pfizer Fellow of the Life Sciences Research Foundation.
** To whom correspondence should be addressed. Tel.: 214-648-1189; Fax: 214-648-1196; E-mail: eolson{at}hamon.swmed.edu.
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