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Originally published In Press as doi:10.1074/jbc.M211762200 on December 10, 2002

J. Biol. Chem., Vol. 278, Issue 9, 6838-6847, February 28, 2003
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The Transcriptional Co-activators CREB-binding Protein (CBP) and p300 Play a Critical Role in Cardiac Hypertrophy That Is Dependent on Their Histone Acetyltransferase Activity*

Rosalind J. GustersonDagger §, Elen Jazrawi, Ian M. Adcock, and David S. LatchmanDagger ||

From the Dagger  Institute of Child Health, University College London, 30 Guilford St., London WC1N 1EH and the  National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse St., London SW3 6LY, United Kingdom

The CBP and p300 proteins are transcriptional co-activators that are involved in a variety of transcriptional pathways in development and in response to specific signaling pathways. We have previously demonstrated that the ability of both these factors to stimulate transcription is greatly enhanced by treatment of cardiac cells with the hypertrophic agent phenylephrine (PE). Here, we show that inhibition of either CBP or p300 with antisense or dominant negative mutant constructs inhibits PE-induced hypertrophy as assayed by atrial naturetic protein production, cardiac cell protein:DNA ratio and cell size. Furthermore, we show that overexpression of CBP or p300 can induce hypertrophy and that this effect requires their histone acetyltransferase (HAT) activity. Moreover, we show that PE can directly enhance CBP HAT activity and that artificial enhancement of HAT activity is sufficient to induce hypertrophy. Hence, CBP and p300 play an essential role in hypertrophy induced by PE, and this effect is mediated via PE-induced enhancement of their HAT activity. This is the first time a role for these factors, and their HAT activity, in hypertrophy has been directly demonstrated.

* This work was supported in part by the British Heart Foundation.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by a Ph.D. studentship from the British Heart Foundation.

|| To whom correspondence should be addressed. Tel.: 44-20-7905-2189; Fax: 44-20-7242-8437; E-mail: d.latchman@ich.ucl.ac.uk.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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