Sodium pump alpha-2 subunit (ATP1A2) alleviates cardiomyocyte anoxia-reoxygenation injury via inhibition of endoplasmic reticulum stress-related apoptosis.

Abstract

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.