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Volume 272, Number 34, Issue of August 22, 1997 pp. 21227-21232
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Opposite Effect of Intracellular Ca²⁺ and Protein Kinase C on the Expression of Inwardly Rectifying K⁺ Channel 1 in Mouse Skeletal Muscle

(Received for publication, February 25, 1997, and in revised form, May 28, 1997)

Ki Soon Shin , Jae-Yong Park , Hyockman Kwon , Chin Ha Chung and Man-Sik Kang

From the Department of Molecular Biology and Research Center for Cell Differentiation, Seoul National University, Seoul 151-742, Korea and the  Department of Molecular Biology, Dankook University, Seoul 140-714, Korea

The level of inwardly rectifying K⁺ channel 1 (IRK1) mRNA decreased upon denervation and increased during muscle differentiation in mouse skeletal muscle. To identify the mechanism(s) underlying the regulation of IRK1 mRNA expression, we examined its expression using the well differentiated C2C12 mouse skeletal muscle cell line as a model system. Since nerve-induced muscle activity results in contraction, it was questioned whether the changes in IRK1 expression might be relevant to the increased intracellular calcium that functions as a cytoplasmic messenger in excitation-contraction coupling. Indeed, activation of either L-type calcium channels or ryanodine receptors increased the level of IRK1 mRNA. More directly, ionomycin activated the IRK1 expression in time- and dose-dependent manners, which was abolished by treatment with EGTA. Genistein, a tyrosine kinase inhibitor, also abolished the stimulating effect of ionomycin. Meanwhile, activation of protein kinase C by 12-O-tetradecanoylphorbol acetate (TPA) markedly decreased the level of IRK1 mRNA, which required ongoing protein synthesis. Actinomycin D experiments revealed that ionomycin increased the half-life of IRK1 mRNA from 0.86 to 1.97 h, but TPA decreased it to 0.38 h. However, neither ionomycin nor TPA appreciably altered the rate of IRK1 gene transcription. Based on these observations, we conclude that intracellular calcium and protein kinase C are oppositely involved in the muscle activity-dependent regulation of IRK1 gene expression and that both act at the level of mRNA stability.

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