缝隙连接蛋白43通过调控L型钙电流参与心房肌细胞的电重塑
봉극련접단백43통과조공L형개전류삼여심방기세포적전중소
Cx43 is involved in electrical remodeling of atrial myocytes through regu-lating L-type calcium current
  • 万方数据
    中国病理生理杂志 중국병리생리잡지
    Chinese Journal of Pathophysiology
    2015年 11期 1986-1991 ,共6页

    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

    요방%설옥매%산춘옥%여세용%초정장%진소현%림추웅%양혜%광소연%류효영%주걸저%오서림

    缝隙连接蛋白43%L型钙通道%心房肌细胞%心房纤颤%电重塑 縫隙連接蛋白43%L型鈣通道%心房肌細胞%心房纖顫%電重塑
    봉극련접단백43%L형개통도%심방기세포%심방섬전%전중소
    Connexin 43%L-type calcium channels%Atrial myocytes%Atrial fibrillation%Electrical remodeling
    目的：观察缝隙连接蛋白43（ Cx43）是否通过与L型钙通道共定位，调控L型钙电流，参与房颤（ AF）的发病机制。方法：使用蛋白免疫印迹和实时荧光定量PCR检测AF和窦性心律患者心房组织中Cx43的蛋白和mRNA表达差异；用RNA干扰技术沉默心房肌细胞的Cx43表达，实时荧光定量PCR和全细胞膜片钳实验观察对L型钙通道mRNA表达和L型钙电流的影响；免疫共沉淀和激光共聚焦显微成像观察心房肌细胞中Cx43与L型钙通道是否存在共定位。结果：AF患者心房组织中的Cx43表达明显低于窦性心律患者；干扰Cx43表达可明显抑制L型钙电流和L型钙通道α1c亚基的mRNA表达；且心房肌细胞中Cx43与L型钙通道存在共定位。结论：心房肌细胞中的Cx43可通过与L型钙通道形成分子复合物，调控L型钙电流，参与心房肌细胞的电重塑。
    목적：관찰봉극련접단백43（ Cx43）시부통과여L형개통도공정위，조공L형개전류，삼여방전（ AF）적발병궤제。방법：사용단백면역인적화실시형광정량PCR검측AF화두성심률환자심방조직중Cx43적단백화mRNA표체차이；용RNA간우기술침묵심방기세포적Cx43표체，실시형광정량PCR화전세포막편겸실험관찰대L형개통도mRNA표체화L형개전류적영향；면역공침정화격광공취초현미성상관찰심방기세포중Cx43여L형개통도시부존재공정위。결과：AF환자심방조직중적Cx43표체명현저우두성심률환자；간우Cx43표체가명현억제L형개전류화L형개통도α1c아기적mRNA표체；차심방기세포중Cx43여L형개통도존재공정위。결론：심방기세포중적Cx43가통과여L형개통도형성분자복합물，조공L형개전류，삼여심방기세포적전중소。
    AIM:To investigate whether the association of connexin 43 ( Cx43 ) and L-type calcium channel involved in the pathogenesis of atrial fibrillation ( AF) .METHODS:The biochemical assays and whole-cell patch-clamp technique were used to study the expression of Cx43 in human atrial tissue.The co-localization of Cx43 and L-type calcium channel, and the regulation of L-type calcium current in atrial myocytes were investigated.RESULTS:The expression of Cx43 at mRNA and protein levels was decreased in human atrial tissues of AF patients.In cultured atrium-derived myocytes ( HL-1 cells) , knockdown of Cx43 significantly inhibited the mRNA expression of L-type calcium channelα1c subunit, as well as L-type calcium current.Co-localization of Cx43 with L-type calcium channel α1c subunit in mouse atrial myocytes was observed.CONCLUSION:The decrease in Cx43 is involved in the pathogenesis of AF, probably through reducing the L-type calcium current in atrial myoctyes by co-localization with L-type calcium channel, thus representing the potential pathogenesis in atrial fibrillation.
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