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Abstract Regulation of voltage-gated K + channel genes represents an important mechanism for modulating cardiac excitability. Here we demonstrate that expression of two K + channel mRNAs is reciprocally controlled by cell-cell interactions between adult cardiac myocytes. It is shown that culturing acutely dissociated rat ventricular myocytes for 3 h results in a dramatic downregulation of Kv1.5 mRNA and a modest upregulation of Kv4.2 mRNA. These effects are specific, because similar changes are not detected with other channel mRNAs. Increasing myocyte density promotes maintenance of Kv1.5 gene expression, whereas Kv4.2 mRNA expression was found to be inversely proportional to cell density. Conditioned culture medium did not mimic the effects of high cell density. However, paraformaldehyde-fixed myocytes were comparable to live cells in their ability to influence K + channel message levels. Thus the reciprocal effects of cell density on the expression of Kv1.5 and Kv4.2 genes are mediated by direct contact between adult cardiac myocytes. These findings reveal for the first time that cardiac myocyte gene expression is influenced by signaling induced by cell-cell contact. voltage-gated K + channel rat ventricular myocyte gene expression Footnotes Address for reprint requests: E. S. Levitan, E1351 Biomedical Science Tower, Dept. of Pharmacology, University of Pittsburgh, Pittsburgh, PA 15261. This work was supported by National Heart, Lung, and Blood Institute (NHLBI) Grant HL-55312 and a Grant-in-Aid from the American Heart Association (Pennsylvania Affiliate). K. M. Hershman was supported by individual NHLBI Postdoctoral Fellowship Grant HL-09347. E. S. Levitan is an Established Investigator of the American Heart Association. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1998 the American Physiological Society
AJP - Cell Physiology – The American Physiological Society
Published: Dec 1, 1998
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