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与震颤相关的钾通道Kv1.4在培养的大鼠心肌细胞中的mRNA调控以及Kv1.4和Kv1.5基因在心肌发育和肥大中的差异表达。

Shaker-related potassium channel, Kv1.4, mRNA regulation in cultured rat heart myocytes and differential expression of Kv1.4 and Kv1.5 genes in myocardial development and hypertrophy.

作者信息

Matsubara H, Suzuki J, Inada M

机构信息

Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan.

出版信息

J Clin Invest. 1993 Oct;92(4):1659-66. doi: 10.1172/JCI116751.

DOI:10.1172/JCI116751
PMID:7691883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC288324/
Abstract

The multiple K+ channels are crucial for repolarization and configuration of the action potential in the neuronal and cardiac cells. In this study, we report the regulatory mechanisms of rapidly inactivating Shaker Kv1.4 channel transcript in the rat heart. Quantitative PCR analysis showed that stimulation with high concentration of KCl, BAY-K 8644, or 12-O-tetradecanoyl phorbol-13-acetate resulted in an immediate and substantial increase (two- to threefold) of Kv1.4 mRNA levels in spontaneously beating myocytes prepared from neonatal rat ventricles. The Kv1.4 mRNA in the ventricle remains at a steady state level after birth and gradually declines with maturation. These results suggest that the Kv1.4 mRNA level is not static and undergoes dynamic modulation by multiple factors that activate intracellular signals. In addition, the expression patterns of Kv1.4 as well as the delayed rectifier Shaker K+ channel Kv1.5 mRNAs were examined in hypertrophied ventricles in which a plateau phase of action potential is remarkably prolonged. The Kv1.5 mRNA level was dramatically repressed while the Kv1.4 mRNA level was remarkably increased. This differential regulation was completely reversed by the normalization of hypertrophy, suggesting that the pathological alterations of K+ channel gene regulation may be involved in the occurrence of ventricular arrhythmias in hypertrophic hearts.

摘要

多种钾离子通道对于神经元和心脏细胞动作电位的复极化和形态形成至关重要。在本研究中，我们报告了大鼠心脏中快速失活的Shaker Kv1.4通道转录本的调控机制。定量PCR分析表明，用高浓度氯化钾、BAY-K 8644或12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯刺激新生大鼠心室制备的自发搏动心肌细胞，会导致Kv1.4 mRNA水平立即大幅增加（两到三倍）。心室中的Kv1.4 mRNA在出生后保持稳定水平，并随着成熟逐渐下降。这些结果表明，Kv1.4 mRNA水平并非静止不变，而是受到激活细胞内信号的多种因素的动态调节。此外，在动作电位平台期显著延长的肥厚心室中检测了Kv1.4以及延迟整流器Shaker钾离子通道Kv1.5 mRNA的表达模式。Kv1.5 mRNA水平显著下调，而Kv1.4 mRNA水平显著上调。肥厚恢复正常后，这种差异调节完全逆转，表明钾离子通道基因调控的病理改变可能参与了肥厚性心肌病中心律失常的发生。

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