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Am J Physiol Heart Circ Physiol 284: H268-H276, 2003. First published September 26, 2002; doi:10.1152/ajpheart.00707.2002
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Vol. 284, Issue 1, H268-H276, January 2003

Alterations in apoptotic signaling in human idiopathic cardiomyopathic hearts in failure

Charles Steenbergen1,*, Cynthia A. Afshari2,*, John G. Petranka3, Jennifer Collins2, Karla Martin2, Lee Bennett2, Astrid Haugen2, Pierre Bushel2, and Elizabeth Murphy3

1 Department of Pathology, Duke University Medical Center, Durham 27710; and 2 Microarray Center and 3 Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709

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 the study of human heart tissue. In this study, we used DNA microarray profiling to investigate changes in the 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 proapoptotic shift in the TNF-alpha signaling pathway. Specifically, we found decreased expression of TNF-alpha - and NF-kappa B-induced antiapoptotic genes such as growth arrest and DNA damage-inducible (GADD)45beta , 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 Ser-112. This study identifies several pathways that are altered in human heart failure and provides new targets for therapy.

TNF-alpha ; GADD45beta ; BAD; gene profiling

* C. Steenbergen and C. A. Afshari contributed equally to this work.




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