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PMID:15367668
| Citation |
Chang, S, McKinsey, TA, Zhang, CL, Richardson, JA, Hill, JA and Olson, EN (2004) Histone deacetylases 5 and 9 govern responsiveness of the heart to a subset of stress signals and play redundant roles in heart development. Mol. Cell. Biol. 24:8467-76 |
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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 beta-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. |
| Links |
PubMed PMC516756 Online version:10.1128/MCB.24.19.8467-8476.2004 |
| Keywords |
Animals; Calcineurin/metabolism; Cardiomegaly/genetics; Cardiomegaly/metabolism; Carrier Proteins/genetics; Carrier Proteins/metabolism; Genes, Reporter; Heart/embryology; Histone Deacetylases/genetics; Histone Deacetylases/metabolism; Mice; Mice, Knockout; Mutation; Myocardium/metabolism; Repressor Proteins/genetics; Repressor Proteins/metabolism |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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