细胞凋亡
切碎
内质网
化学
转染
分子生物学
半胱氨酸蛋白酶3
药理学
医学
生物
生物化学
程序性细胞死亡
基因
作者
Yu-Long Hu,Zheng Wang,Nannan Ge,Ting Huang,Mingchao Zhang,Hegui Wang
标识
DOI:10.1139/cjpp-2017-0349
摘要
Previous studies have found decreased functional capacity of the sodium pump (Na + -K + -ATPase) alpha and beta subunits and recovery of Na + -K + -ATPase activity significantly decreased myocyte apoptosis in myocardial ischemia–reperfusion (I/R) injury. However, the potential role of the Na + -K + -ATPase α-2 subunit (ATP1A2) in cardiomyocyte anoxia–reoxygenation (A/R) injury has not been elucidated. Rat myocardial cells were subjected to siRNA transfection followed by A/R injury. Apoptosis and expression of endoplasmic reticulum (ER) stress proteins CHOP, GRP78, and caspase-12 were detected in 4 groups of cells: ATP1A2 siRNA + A/R, control siRNA + A/R, control, and A/R injury model. We found that apoptosis was significantly elevated in the ATP1A2 siRNA + A/R group as compared with control siRNA + A/R, control, and A/R injury model groups (p < 0.05, p < 0.01, and p < 0.05). Furthermore, expression of CHOP, GRP78, and caspase-12 were significantly elevated in the ATP1A2 siRNA + A/R group as compared with control siRNA + A/R, control, and A/R injury model groups (p < 0.05, p < 0.01, and p < 0.05). Our findings suggest that cardiomyocyte ATP1A2 is a target of A/R injury, and its cardioprotective function may be mediated via inhibiting the ER-stress-related apoptosis.
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