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Am J Physiol Cell Physiol 278: C397-C403, 2000;
0363-6143/00 $5.00
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Vol. 278, Issue 2, C397-C403, February 2000

RPTPµ and protein tyrosine phosphorylation regulate K+ channel mRNA expression in adult cardiac myocytes

Kenneth M. Hershman and Edwin S. Levitan

Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

Previously, we reported that cell-cell contact regulates K+ channel mRNA expression in cultured adult rat cardiac myocytes. Here we show that exposing cardiac myocytes to tyrosine kinase inhibitors (genistein, tyrphostin A25), but not inactive analogs, prevents downregulation of Kv1.5 mRNA and upregulation of Kv4.2 mRNA normally observed when they are cultured under low-density conditions. Furthermore, cardiac myocytes cocultured with cells that endogenously (Mv 1 Lu) or heterologously (Chinese hamster ovary cells) express the receptor-type protein tyrosine phosphatase µ (RPTPµ) display Kv1.5 mRNA levels paralleling that which was observed in myocytes cultured under high-density conditions and in intact tissue. In contrast, myocytes cocultured with control cells failed to produce this response. Finally, it is shown that Kv4.2 mRNA expression is unaffected by RPTPµ. These findings reveal that multiple tyrosine phosphorylation-dependent mechanisms control cardiac myocyte K+ channel genes. Furthermore, we conclude that RPTPµ specifically regulates cardiac myocyte Kv1.5 mRNA expression. Thus this receptor protein tyrosine phosphatase may be important in responses to pathological conditions associated with the loss of cell-cell interactions in the heart.

receptor-type protein tyrosine phosphatase µ; cell-cell contact; rat ventricular myocyte; voltage-gated potassium channel; gene expression


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