Yang Long, Deng Na, He Jionghong, Xia Guiling, Yang Ying, Zhao Yidong, Huo Zhaomei, Guo Chuxian
Department of Cardiology, Guizhou Provincial People's Hospital, No. 83 Zhongshandong Road, Guiyang 550002, China.
Department of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550025, China.
Open Life Sci. 2021 Sep 21;16(1):1010-1021. doi: 10.1515/biol-2021-0107. eCollection 2021.
It has been shown that the activation of calcineurin is involved in regulating ion channel remodeling in hypertrophic cardiomyocytes. But the precise role of calcineurin in the regulation of transient outward potassium current ( ), an ion channel associated with fatal arrhythmia, remains controversial. This study aimed to examine the effects of () gene knockdown on channel remodeling and action potential duration (APD) in the hypertrophic ventricular myocytes of neonatal rats. Results showed that phenylephrine stimulation caused hypertrophy of ventricular myocytes, upregulation of CnAβ protein expression, downregulation of mRNA and protein expression, a decrease in current density, and prolongation of APD. gene knockdown significantly inhibited the effects of phenylephrine stimulation. Our data indicate that gene knockdown can inhibit channel remodeling and APD prolongation in hypertrophic neonatal rat ventricular myocytes. This finding suggests that calcineurin may be a potential target for the prevention of malignant ventricular arrhythmia in a hypertrophic heart.
研究表明，钙调神经磷酸酶的激活参与调节肥厚型心肌细胞中的离子通道重塑。但是，钙调神经磷酸酶在调节瞬时外向钾电流（一种与致命性心律失常相关的离子通道）中的确切作用仍存在争议。本研究旨在检测钙调神经磷酸酶Aβ（CnAβ）基因敲低对新生大鼠肥厚型心室肌细胞中瞬时外向钾电流（Ito）通道重塑和动作电位时程（APD）的影响。结果显示，苯肾上腺素刺激导致心室肌细胞肥大、CnAβ蛋白表达上调、Ito mRNA和蛋白表达下调、Ito电流密度降低以及APD延长。CnAβ基因敲低显著抑制了苯肾上腺素刺激的作用。我们的数据表明，CnAβ基因敲低可抑制新生大鼠肥厚型心室肌细胞中的Ito通道重塑和APD延长。这一发现提示，钙调神经磷酸酶可能是预防肥厚型心脏恶性室性心律失常的一个潜在靶点。
