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Physiol. Genomics 6: 19-28, 2001;
1094-8341/01 $5.00
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Received 6 October 2000; accepted in final form 5 April 2001.
Physiological Genomics 6:19-28 (2001)
1094-8341/01 $5.00 © 2001 American Physiological Society

Divergent transcriptional responses to independent genetic causes of cardiac hypertrophy

BRUCE J. ARONOW1, TSUYOSHI TOYOKAWA2, AMY CANNING2, KOBRA HAGHIGHI3, ULRIKE DELLING4, EVANGELIA KRANIAS3, JEFFERY D. MOLKENTIN4 and GERALD W. DORN, II2,3

1 Departments of Developmental Biology
4 Molecular Cardiovascular Biology, Children’s Hospital Research Center, Cincinnati 45229; and the
2 Division of Cardiology
3 Department of Pharmacology and Cell Therapeutics, University of Cincinnati Medical Center, Cincinnati, Ohio 45267-0542

To define molecular mechanisms of cardiac hypertrophy, genes whose expression was perturbed by any of four different transgenic mouse hypertrophy models [protein kinase C-{epsilon} activation peptide ({Psi}{epsilon}RACK), calsequestrin (CSQ), calcineurin (CN), and G{alpha}q] were compared by DNA microarray analyses using the ~8,800 genes present on the Incyte mouse GEM1. The total numbers of regulated genes (tens to hundreds) correlated with phenotypic severity of the model (G{alpha}q > CN > CSQ > {Psi}{epsilon}RACK), but demonstrated that no single gene was consistently upregulated. Of the three models exhibiting pathological hypertrophy, only atrial natriuretic peptide was consistently upregulated, suggesting that transcriptional alterations are highly specific to individual genetic causes of hypertrophy. However, hierarchical-tree and K-means clustering analyses revealed that subsets of the upregulated genes did exhibit coordinate regulatory patterns that were unique or overlapping across the different hypertrophy models. One striking set consisted of apoptotic genes uniquely regulated in the apoptosis-prone G{alpha}q model. Thus, rather than identifying a single common hypertrophic cardiomyopathy gene program, these data suggest that extensive groups of genes may be useful for the prediction of specific underlying genetic determinants and condition-specific therapeutic approaches.

cardiac hypertrophy; transgenic mouse; gene expression; DNA microarray




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