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Down-regulation of Cav1.2 by its Regulating Protein Calpastatin in Myocardial Hypoxic-Ischemic Injury

胡慧媛  毛楠  晏珊  孙宇  王健  王莹  孙雪菲  赵金生  郝丽英  
【摘要】:Our recent study has revealed that calpastatin,an endogenous calpain inhibitor,could not only reprime activity of Cav1.2 Ca2+channel from run-down in cell-free patches but also directly bind to intracellular C-terminal region of Cav1.2 channel.However,the pathophysiological role of Cav1.2-channel-regulating function of calpastatin was largely unknown.In this study,we investigated the changes in expression and function of Cav1.2 channels associated with calpastatin in both in vitro H9c2 hypoxia model and in vivo myocardial infarction(MI)model of rats.We found that both m RNA and protein levels of Cav1.2 and calpastatin decreased at the late stage of hypoxic-ischemic(H-I)injury,which could not be prevented by administration of calpain inhibitor MDL 28170.At the same time,influx of Ca2+induced by KCl wasattenuated in H9c2 cells confronted to hypoxia.In addition,colocalization of Cav1.2 and calpastatin on the cytoplasmic membrane was observed in sham-operated rats,but it was only detected in cytosol in rats encountered MI.Knockdown of calpastatin with si RNA in H9c2 cells resulted in both decreased Cav1.2 levels and depressed Cav1.2 channel activity.Taken together,these results indicate that dysregulation of Cav1.2 Ca2+channel by calpastatin was involved in myocardial H-I injury,which provide insights that proper regulation of Cav1.2 Ca2+channel by calpastatin was needed in maintaining the normal cardiac function.

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