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Physiol. Genomics (November 12, 2002). doi:10.1152/physiolgenomics.00148.2002
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Articles in PresS, published online ahead of print November 12, 2002
Physiol Genomics, 10.1152/physiolgenomics.00148.2002
Submitted on November 4, 2002
Accepted on November 11, 2002

Transcriptomal analysis of failing and non-failing human hearts

Marja Steenman1*, Yi-Wen Chen2, Martine Le Cunff1, Guillaume Lamirault1, Andras Varro3, Eric Hoffman2, and Jean J Leger1

1 INSERM U533, Nantes, France
2 Children's National Medical Center, Washington, DC, USA
3 Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary

* To whom correspondence should be addressed. E-mail: marja.steenman{at}nantes.inserm.fr.

Heart failure is a multifactorial disease that may result from different initiating events. In order to contribute to an improved comprehension of normal cardiac function and the molecular events leading to heart failure, we performed large-scale gene expression analysis of failing and non-failing human ventricle. The aim of our study was to define and to compare the expression profiles of 4 specific pathophysiological cardiac situations: 1) left ventricle from non-failing heart; 2) left ventricle from failing hearts affected by dilated cardiomyopathy; 3) left ventricle from failing hearts affected by ischemic cardiomyopathy; 4) right ventricle from failings hearts affected by dilated or ischemic cardiomyopathy. We used oligonucleotide-arrays representing ~12,000 human genes. After stringent numerical analyses using several statistical tests, we identified 1306 genes with a similar expression profile in all 4 cardiac situations, therefore being representative of part of the human cardiac expression profile. A total of 95 genes displayed differential expression between failing and non-failing heart samples, reflecting a reversal to developmental gene expression, dedifferentiation of failing cardiomyocytes and involvement of apoptosis. Twenty genes were differentially expressed between failing left and failing right ventricle, identifying possible candidates for different functioning of both ventricles. Finally, no genes were found to be significantly differentially expressed between failing dilated and failing ischemic left ventricle, underlining the fact that transcriptomal analysis of explanted hearts results mainly in the identification of expression profiles of end-stage heart failure and less in the determination of expression profiles of the underlying etiology. Taken together, our data resulted in the identification of putative transcriptomal landmarks for normal and disturbed cardiac function.




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