β_2受体对心肌缝隙连接蛋白Cx43的调节  

Regulation of β_2-adrenergic receptor stimulation on gap junction protein connexin 43 in cultured rat cardiomyocytes.

作　　者：夏益[1] 张萍[1] 宋娆[2] 吕志珍[2] 张幼怡[2] 郭继鸿[1] 

机构地区：[1]北京大学人民医院心脏中心,100044 [2]北京大学第三医院血管医学研究所,100083

出　　处：《临床心电学杂志》2008年第2期122-125,共4页Journal of Clinical Electrocardiology

基　　金：国家自然科学基金项目(项目编号30471916);北京市自然科学基金项目(项目编号7052045)

摘　　要：目的探讨β-肾上腺素受体(β-AR)亚型对心肌缝隙连接蛋白connexin 43(Cx43)表达及功能的调节。方法采用免疫印迹技术和划痕标记示踪技术(SLDT)观察心肌细胞Cx43的表达和功能变化。结果给予异丙基肾上腺素(ISO)刺激5min,即可明显增加心肌细胞非磷酸化Cx43的表达,同时促进荧光染料在细胞间的扩散;选择性β2-AR拮抗剂ICI 118551,可完全拮抗异丙基肾上腺素所诱导的该作用。结论异丙基肾上腺素主要通过刺激β2-AR参与调控Cx43,这可能是β2-AR诱导心律失常的一个重要机制。Objective To investigate the effects of β2-AR stimulation on Cx43 expression and gap junction intercellular communication （GJIC） function. Methods In cultured neonatal rat cardiac myocytes, we use the Western blotting assay and scrape loading/dye transfer assay （SLDT） to detect the expression of Cx43 and the function 0f GJIC. Results stimulation of β2-AR agonist isoproterenol for 5 minutes quickly induced the up-regulation of expression of nonphosphorylated Cx43 （Cx43-NP）. In addition, we observed the enhancement of GJIC by SLDT. A selective β2-adrenergic inhibitor ICI 118551 could fully abolish the effect. Conclusions These results suggested β2-AR stimulation increase the expression of Cx43-NP, and meanwhile enhance the gating function of gap junctions in cardiac myocytes. The regulatory effect of Cx43 expression may be a potential mechanism of alternated cardiac eleetrophysiologic properties by β2-AR agonist.

关 键 词：CX43 缝隙连接蛋白 β2 肾上腺素受体 心肌细胞 

分 类 号：R541[医药卫生—心血管疾病]