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Pro)renin receptor (PRR) contributes to regulating many physiological and
pathological processes; however, the role of PRR-mediated signaling pathways in
myocardial ischemia/
reperfusion injury (IRI) remains unclear. In this study, we used an in vitro model of
hypoxia/reoxygenation (H/R) to mimic IRI and carried out PRR knockdown by
siRNA and PRR overexpression using
cDNA in H9c2 cells. Cell proliferation activity was examined by MTT and Cell Counting Kit-8 (CCK-8) assays. Apoptosis-related factors, autophagy markers and
beta-catenin pathway activity were assessed by real-time PCR and western blotting. After 24 h of
hypoxia followed by 2 h of reoxygenation, the expression levels of PRR, LC3B-I/II,
Beclin1, cleaved
caspase-3, cleaved
caspase-9 and Bax were upregulated, suggesting that apoptosis and autophagy were increased in H9c2 cells. Contrary to the effects of PRR downregulation, the overexpression of PRR inhibited proliferation, induced apoptosis, increased the expression of pro-apoptotic factors and autophagy markers, and promoted activation of the
beta-catenin pathway. Furthermore, all these effects were reversed by treatment with the
beta-catenin antagonist DKK-1. Thus, we concluded that PRR activation can trigger H/R-induced apoptosis and autophagy in H9c2 cells through the
beta-catenin signaling pathway, which may provide new therapeutic targets for the prevention and treatment of myocardial IRI.