模拟失重对大鼠心肌组织缝隙连接蛋白表达谱的影响

发布时间：2018-12-24 13:44

【摘要】：目的研究模拟失重对大鼠心肌组织缝隙连接蛋白(CX)亚型表达谱的影响,为探讨模拟失重条件下心律失常部分发生机制提供新的实验依据。方法将20只成年雄性Wistar大鼠随机平均分为正常对照组(Con)及尾部悬吊模拟失重组(SUS),应用电子透射电镜检测大鼠心肌组织超微结构,RT-PCR、Western bloting检测连接蛋白CX37、CX40、CX43、CX45mRNA及CX40、CX43、CX45蛋白表达水平。结果与Con组相比,模拟失重可致部分心肌细胞肌纤维变性,线粒体变性、数量减少,胶原增多,局部间隙连接增宽、结构消失。RT-PCR结果显示,SUS组心肌组织CX各亚型mRNA表达水平普遍显著下降,Western bloting结果显示,模拟失重条件下,CX43和CX45蛋白表达水平亦显著下降。结论模拟失重2wk,大鼠心肌组织超微结构发生明显改变,缝隙连接出现非均质性结构变化,心肌组织缝隙连接蛋白表达谱普遍下调。结果提示,失重可以导致心肌缝隙连接蛋白重构,其可能影响心肌细胞间电兴奋传导的速度及方向,从而使传导阻滞和微折返易于出现,诱发心律失常。
[Abstract]:Objective to study the effect of simulated weightlessness on the expression profile of gap junction protein (CX) subtype in rat myocardial tissue, and to provide a new experimental basis for exploring the mechanism of arrhythmia in simulated weightlessness. Methods Twenty adult male Wistar rats were randomly divided into normal control group (Con) and tail suspension simulated weightlessness group (SUS),). The ultrastructure of myocardial tissue was detected by electron transmission electron microscopy (TEM), and the junction protein CX37,CX40, (CX37,CX40,) was detected by RT-PCR,Western bloting. CX43,CX45mRNA and CX40,CX43,CX45 protein expression level. Results compared with Con group, simulated weightlessness could result in the degeneration of myofibril, mitochondria degeneration, decrease in quantity, increase of collagen, widening of local gap junction and disappearance of structure in some cardiomyocytes. The expression of CX subtypes mRNA in SUS group was significantly decreased. The results showed that under simulated weightlessness, the expression levels of CX43 and CX45 protein also decreased significantly. Conclusion after simulated weightlessness for 2 wk, the ultrastructure of myocardial tissue changed obviously, the gap junction showed heterogeneity, and the expression profile of gap junction protein was down-regulated. The results suggest that weightlessness can lead to the remodeling of gap junction protein, which may affect the velocity and direction of electrical excitatory conduction between myocardial cells, thus making conduction block and microreentry easy to appear and induce arrhythmia.
【作者单位】：西安交通大学医学院生理学与病理生理学系中国航天员科研训练中心中国航天员科研训练中心中国航天员科研训练中心中国航天员科研训练中心中国航天员科研训练中心西安交通大学医学院生理学与病理生理学系
【基金】：国家自然科学基金资助(30400158)
【分类号】：R852.22

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