MeCP2 attenuates cardiomyocyte hypoxia/reperfusion-induced injury via regulation of the SFRP4/Wnt/β-catenin axis.

Methylated CpG binding protein 2 (MeCP2) is closely associated with heart failure, but its role in I/R injury remains unclear. The purpose of this study was to explore the role and underling mechanism of MeCP2 in myocardial I/R injury. Hypoxia/reperfusion (H/R)-induced H9c2 cardiomyocytes was used to establish an I/R injury model. Oxidative stress was assessed by measuring reactive oxygen species (ROS) generation, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity. Cell viability and cell cycle arrest were evaluated by the Cell Counting Kit-8 assay and cell cycle assay, respectively. Apoptosis was determined using flow cytometry analysis. The expression of MeCP2 in H9c2 cells was decreased after H/R treatment. The overexpression of MeCP2 inhibited H/R-induced oxidative stress, cell cycle arrest and apoptosis of H9c2 cells. Moreover, MeCP2 inhibited the activation of secreted frizzled related protein 4 (SFRP4)/Wnt/β-catenin axis, and SFRP4 relieved the effect of MeCP2 on oxidative stress, cell cycle arrest and apoptosis in H/R-induced H9c2 cells. MeCP2 attenuated H/R-induced injury in H9c2 cardiomyocytes by modulating the SFRP4/Wnt/β-catenin axis, which suggested that MeCP2 might serve as a therapeutic target of patients with AMI after reperfusion.