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MAMMALIAN GENETIC MODELS WITH MINIMAL OR COMPLEX PHENOTYPES

Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development

Shurong Chang, Timothy A. McKinsey, Chun Li Zhang, James A. Richardson, Joseph A. Hill, Eric N. Olson
Shurong Chang
1Departments of Molecular Biology
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Timothy A. McKinsey
2Myogen, Inc., Westminster, Colorado
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Chun Li Zhang
1Departments of Molecular Biology
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James A. Richardson
1Departments of Molecular Biology
3Pathology
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Joseph A. Hill
1Departments of Molecular Biology
4Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas
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Eric N. Olson
1Departments of Molecular Biology
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  • For correspondence: eolson@hamon.swmed.edu
DOI: 10.1128/MCB.24.19.8467-8476.2004
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ABSTRACT

The adult heart responds to stress signals by hypertrophic growth, which is often accompanied by activation of a fetal cardiac gene program and eventual cardiac demise. We showed previously that histone deacetylase 9 (HDAC9) acts as a suppressor of cardiac hypertrophy and that mice lacking HDAC9 are sensitized to cardiac stress signals. Here we report that mice lacking HDAC5 display a similar cardiac phenotype and develop profoundly enlarged hearts in response to pressure overload resulting from aortic constriction or constitutive cardiac activation of calcineurin, a transducer of cardiac stress signals. In contrast, mice lacking either HDAC5 or HDAC9 show a hypertrophic response to chronic β-adrenergic stimulation identical to that of wild-type littermates, suggesting that these HDACs modulate a specific subset of cardiac stress response pathways. We also show that compound mutant mice lacking both HDAC5 and HDAC9 show a propensity for lethal ventricular septal defects and thin-walled myocardium. These findings reveal central roles for HDACs 5 and 9 in the suppression of a subset of cardiac stress signals as well as redundant functions in the control of cardiac development.

  • Copyright © 2004 American Society for Microbiology
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Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development
Shurong Chang, Timothy A. McKinsey, Chun Li Zhang, James A. Richardson, Joseph A. Hill, Eric N. Olson
Molecular and Cellular Biology Sep 2004, 24 (19) 8467-8476; DOI: 10.1128/MCB.24.19.8467-8476.2004

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Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development
Shurong Chang, Timothy A. McKinsey, Chun Li Zhang, James A. Richardson, Joseph A. Hill, Eric N. Olson
Molecular and Cellular Biology Sep 2004, 24 (19) 8467-8476; DOI: 10.1128/MCB.24.19.8467-8476.2004
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KEYWORDS

Carrier Proteins
heart
Histone Deacetylases
Myocardium
Repressor Proteins

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