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Cardiovascular Research 2003 57(2):477-485; doi:10.1016/S0008-6363(02)00703-4
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Genetic basis for chamber-specific ventricular phenotypes in the rat infarct model

Sumeet S Chugha,*, Stacey Whitesela, Mark Turnerb, Charles T Roberts, Jr.b and Srinivasa R Nagallab

aDivision of Cardiology, Department of Medicine, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA
bDepartment of Pediatrics, Oregon Health and Science University, Portland OR, USA

chughs{at}ohsu.edu

* Corresponding author. Fax: +1-503-494-8750

Background: We, and others, have previously reported a strong correlation between increased inter-ventricular dispersion of repolarization and the occurrence of fatal arrhythmia in animal models of CHF. The existence of this and other such distinct electrophysiologic phenotypes in right (RV) vs. left ventricles (LV) could be explained by chamber-specific patterns of gene expression. Methods: We employed microarray gene profiling of 13 824 sequence-verified, nonredundant rodent cDNAs to compare myocardial gene expression in RV vs. LV of rats with surgically induced myocardial infarction (MI: n=3) and in sham-operated animals (Sham: n=3). Results: Significant LV infarction (32±4% LV) and severe CHF were observed in all MI animals at 4 weeks. In Sham animals, 937 genes exhibited significant differential expression in RV vs. LV myocardium. In MI animals, 1158 genes exhibited significant differential expression in RV vs. LV. Of those genes exhibiting significant differential expression, only 241 were common to both Sham and MI animals. Differentially expressed genes included those involved in signal transduction, cell growth and maintenance, and apoptosis. Genes with potential roles in altered dispersion of repolarization included voltage-dependent Ca2+ channel {gamma} subunit (MI 8-fold{uparrow}) and K+ inwardly rectifying channel subfamily J, member 10 (MI 6-fold{downarrow}). Gap junction membrane channel protein {alpha} 4 (MI 6-fold{downarrow}) and cardiac troponin I (MI 8-fold{downarrow}) were also significantly differentially expressed. Inter-ventricular comparisons revealed significantly greater alterations in gene expression vs. intra-ventricular comparisons. Conclusions: Microarray gene profiling has revealed candidate genes, some of them novel, which may account for chamber-specific ventricular electrophysiologic phenotypes, both in physiologic as well as in arrhythmogenic states such as CHF.

KEYWORDS Arrhythmia (mechanisms); Gene expression; Heart failure; Infarction; Ion channels; Repolarization; Sudden death


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