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.

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.