Connexin 43 co-locolizes and regulates the L type calcium channel current in atrial myocytes

作     者：饶芳 薛玉梅 邓春玉 余细勇 肖定璋 陈少贤 林秋雄 杨慧 邝素娟 刘晓颖 朱杰宁 吴书林 

作者机构：Department of Cardiology Guangdong Cardiovascular Institute Research Center of Medical Sciences Guangdong General Hospital Guangdong Academy of Medical Sciences 

出 版 物：《South China Journal of Cardiology》 (岭南心血管病杂志（英文版）)

年 卷 期：2015年第16卷第2期

页      面：114-121页

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：supported by National Natural Science Foundation of China(No.81470440) Guangdong Natural Science Foundation(No.S2013010016256) Medical Scientific Research Foundation of Guangdong Province(No.A2013049) 

主　　题：connexin 43 L type calcium channel current HL-1 cells atrial fibrillation 

摘      要：Background Atrial fibrillation （AF） is the most common sustained cardiac arrhythmia without effective treatment. AF is associated with atrial conduction disturbances caused by electrical and / or structural remodeling. But the role of connexin （Cx） 43 in the regulation of L type calcium channel （LCC） remains unclear. We hypothesized that Cx 43 might co-localize and regulate the L type calcium channel current （ICa, D. Methods Real-time PCR and whole-cell patch clamp were used to detect the expression of LCC lc subunit and the cur rent density of Ica, L, before and after Cx 43 knocking down respectively. The co-localization of Cx 43 with LCC was investigated by co-immunoprecipitation and confocal microscopy. Results Knocking down of Cx43 significantly inhibited the current density of ICa, L through decreasing the gene expression of LCC alc in cul tured atrium-derived myocytes （HL-1 cells）. Cx43 co-localized with LCC eric subunit in atrial myocytes. Conclusions Cx 43 regulates the ICa, L in atrial myoctyes through LCC, representing a potential pathogenic mechanism in atrial arrhythmias.