Absence of Rgs5 prolongs cardiac repolarization and predisposes to ventricular tachyarrhythmia in mice
Absence of Rgs5 prolongs cardiac repolarization and predisposes to ventricular tachyarrhythmia in mice
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Rgs5 缺失会延长小鼠心脏复极时间并诱发室性快速心律失常
DOI：
10.1016/j.yjmcc.2012.10.003
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发表时间：
2012-12-01
影响因子：
5
通讯作者：
Huang, Congxin
中科院分区：
文献类型：
--
作者：
Qin, Mu;Huang, He;Huang, Congxin
本研究的目的是阐明G蛋白信号负调节因子Rgs 5对小鼠心脏复极和心律失常的影响。对野生型和Rgs 5（-/-）小鼠进行体内、体外和细胞电生理学实验。Rgs 5（-/-）小鼠心脏表现出显著延长的心脏复极，包括延长的QT间期和动作电位时程（APD）。与这些发现一致，Rgs 5（-/-）小鼠心室肌细胞K+电流的测量显示与野生型小鼠相比，外向电压依赖性K+电流（包括I-peak、I-to、I-Kur和I-ss）显著降低。与野生型小鼠相比，Rgs 5（-/-）小鼠心室中Kv4.2、Kv4.3、Kv1.5和Kv2.1的转录和蛋白表达水平下调（P
The aim of this study was to elucidate the effects of regulator of G-protein signaling 5 (Rgs5), a negative regulator of G-protein-mediated signaling, on cardiac repolarization and arrhythmia in mice. Wild-type and Rgs5(-/-) mice were subjected to in vivo, in vitro, and cellular electrophysiological experiments. Rgs5(-/-) mouse hearts showed significantly prolonged cardiac repolarization, including prolonged QT interval and action potential duration (APD). Consistent with these findings, measurement of K+ currents in ventricular myocytes of Rgs5(-/-) mice revealed significant reduction of the outward voltage-dependent K+ currents, including I-peak, I-to, I-Kur, and I-ss, compared to that in wild-type mice. Transcript and protein expression levels of Kv4.2, Kv4.3, Kv1.5, and Kv2.1 were downregulated in Rgs5(-/-) mouse ventricles compared with those in wild-type mice (P