LncRNA MIR17HG alleviates heart failure via targeting MIR17HG/miR-153-3p/SIRT1 axis in in vitro model

Abstract

Abstract Heart failure (HF) is a syndrome of symptoms and signs caused by cardiac insufficiency and have become a serious global health problem. The aim of this study is to clarify the role and mechanism failure of MIR17HG. We established the in vitro HF model by using H2O2-treated AC-16 and HCM cells, and the reactive oxygen species (ROS) level and natriuretic peptide precursor B (NPPB) expression were also detected. The RNA expression of MIR17HG, miR-153-3p, SIRT1, and NPPB were detected by quantitative reverse transcription PCR while the SIRT1 and NPPB expression were detected by western blot. The binding relationship among MIR17HG, miR-153-3p, and SIRT1 were assessed by dual-luciferase reporter assay and RNA binding protein immunoprecipitation assay. Then, MIR17HG and SIRT1 were overexpressed by lentivirus transfection, and the influence of MIR17HG and SIRT1 on H2O2-induced apoptosis mediated by p53 were evaluated. The results show that MIR17HG and SIRT1 were significantly downregulated, while miR-153-3p was significantly upregulated in HF model. Overexpression of MIR17HG reduced miR-153-3p and alleviated HF, while knockdown of SIRT1 weakened the effects of MIR17HG, suggesting that SIRT1 was the direct target of MIR17HG/miR-153-3p axis. MIR17HG is significantly downregulated in HF model. Our research shows that MIR17HG protects cardiomyocytes from ROS-induced damage via the MIR17HG/miR-153-3p/SIRT1 axis, suggesting that MIR17HG and SIRT1 are potential therapeutic targets in HF.