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Am J Physiol Heart Circ Physiol (September 26, 2002). doi:10.1152/ajpheart.00707.2002
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Articles in PresS, published online ahead of print September 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00707.2002
Submitted on August 13, 2002
Accepted on September 20, 2002

Alterations in Apoptotic Signaling in Human Idiopathic Cardiomyopathic Hearts in Failure

Charles Steenbergen1, Cynthia A Afshari1, John G Petranka2, Jennifer Collins1, Karla Martin1, Lee Bennett1, Astrid Haugen1, Pierre Bushel1, and Elizabeth Murphy2*

1 Mircorarray Center, NIEHS, NIH, RTP, NC, USA
2 Laboratory of Signal Transduction, NIEHS, NIH, RTP, NC, USA

* To whom correspondence should be addressed. E-mail: murphy1{at}niehs.nih.gov.

Dilated cardiomyopathy, a disease of unknown etiology and pathogenesis is associated with heart failure and compensatory hypertrophy. Although cell and animal models suggest a role for altered gene expression in the transition to heart failure, there is a paucity of data derived from study of human heart tissue. In this study, we used DNA microarray profiling to investigate changes in expression of genes involved in apoptosis that occur in human idiopathic dilated cardiomyopathic hearts that had progressed to heart failure. We observed altered gene expression consistent with a pro-apoptotic shift in the TNF-{alpha} signaling pathway. Specifically we found decreased expression of the TNF-{alpha} and NF-{kappa}B induced anti-apoptotic genes such as GADD45ß, Flice inhibitory protein (FLIP) and TNF induced protein 3 (A20). Consistent with a role for apoptosis in heart failure, we also observed a significant decrease in phosphorylation of BAD at serine 112. This study identifies several pathways that are altered in human heart failure and provides new targets for therapy.




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