Calmodulin kinase II inhibitor regulates calcium homeostasis changes caused by acute β-adrenergic receptor agonist stimulation in mouse ventricular myocytes
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- 作者：Yan Huang ; Tao Liu ; Dandan Wang ; Xin Wang…
- 关键词：Isoproterenol ; Calmodulin kinase II inhibitor ; IL ; Ca ; Kinetics of L ; type calcium channels ; Ca2+ transient
- 刊名：In Vitro Cellular & Developmental Biology - Animal
- 出版年：2016
- 出版时间：February 2016
- 年：2016
- 卷：52
- 期：2
- 页码：156-162
- 全文大小：1,075 KB
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Tao Liu (1)
Dandan Wang (1)
Xin Wang (1)
Ran Li (1)
Yuting Chen (1)
Yanhong Tang (1)
Teng Wang (1)
Congxin Huang (1)
1. Department of Cardiology, Renmin Hospital of Wuhan University, 99 Zhangzhidong Road, Wuhan, Hubei, 430060, People’s Republic of China - 刊物主题：Cell Biology; Developmental Biology; Stem Cells; Cell Culture; Animal Genetics and Genomics;
- 出版者：Springer US
- ISSN：1543-706X
文摘
Ca2+/calmodulin-dependent kinase II (CaMKII) is an important regulatory molecule under chronic β-adrenergic receptor agonist stimulation but cardiac diseases also occur when β-adrenergic elevated acutely in the circulation, of which the most harmful is lethal arrhythmia. The purpose of this study was to explore the effects of acute isoproterenol (ISO) stimulation on intracellular calcium handling and evaluate whether CaMKII inhibitor may change the effects caused by isoproterenol. Mouse ventricular myocytes were acutely isolated by enzymatic method and divided into four groups: control group, ISO group, KN-93 group, ISO + KN-93 group. The whole-cell patch clamp was used to study the effect of ISO and KN-93 on L-type calcium current (IL-Ca) in isolated ventricular myocytes. The technology of laser scanning confocal microscopy was used to record cardiomyocyte calcium transients after ISO and KN-93 were used. ISO significantly increased current density of IL-Ca (p < 0.01) and decreased the half activation voltage (p < 0.01), half inactivation voltage (p < 0.01), and the recovery time constant (p < 0.01). In the presence of CaMKII inhibitor, KN-93 decreased the increased current density of IL-Ca (p < 0.05), increased the reduced half activation voltage caused by ISO (p < 0.01), and prolonged the shortened recovery time constant caused by ISO (p < 0.01). In addition, KN-93 alone can change the activation, inactivation, and recovery kinetics of L-type calcium channels. Moreover, ISO significantly increased the Ca2+ transient amplitude during both stimulation frequencies (0.5 Hz: p < 0.01, 1 Hz: p < 0.01) and was easy to induce calcium disorders; in the presence of KN-93, these changes were weakened (0.5 Hz: p < 0.05, 1 Hz: p < 0.05). Therefore, changes of the calcium homeostasis in cardiomyocytes caused by ISO can be adjusted by KN-93, thus KN-93 plays a vital role in regulating calcium homeostasis changes caused by ISO. Keywords Isoproterenol Calmodulin kinase II inhibitor IL-Ca Kinetics of L-type calcium channels Ca2+ transient