Circ-SWT1 Ameliorates H2O2-Induced Apoptosis, Oxidative Stress and Endoplasmic Reticulum Stress in Cardiomyocytes via miR-192-5p/SOD2 Axis.

Acute myocardial infarction (AMI) is a most serious cardiovascular disease. Increasing findings have indicated that circular RNAs (circRNAs) serve as competent biomarkers in the process of AMI. Herein, our study aimed to probe the functions of circ-SWT1 in cardiomyocyte injury after AMI. H2O2-induced human cardiomyocyte cell line AC16 were used for expression and function analyses. The levels of genes and proteins were detected by qRT-PCR and western blotting. Cell apoptosis was analyzed by flow cytometry and caspase3 activity analysis. The oxidative stress injury was evaluated by detecting the levels of reactive oxygen species (ROS), malondialdehyde and superoxide dismutase (SOD). Western blotting was used to detect the expressions of apoptosis-related markers and endoplasmic reticulum stress (ERS) markers. Dual-luciferase reporter, RIP and pull-down assays were applied to confirm the interaction between miR-192-5p and circ-SWT1 or SOD2. H2O2 treatment significantly decreased circ-SWT1 expression in cardiomyocytes, functionally, ectopic expression of circ-SWT1 attenuated H2O2-triggered apoptosis, oxidative stress and endoplasmic reticulum (ER) stress in cardiomyocytes in vitro. Mechanistically, circ-SWT1 competitively bound to miR-192-5p to relieve the repression of miR-192-5p on its target SOD2. Further rescue experiments showed that miR-192-5p upregulation reversed the inhibitory effects of circ-SWT1 on H2O2-induced cardiomyocyte injury. Moreover, miR-192-5p inhibition protected cardiomyocytes against H2O2-evoked apoptosis, oxidative stress and ER stress, which were abolished by SOD2 silencing. Circ-SWT1 ameliorates H2O2-induced apoptosis, oxidative stress and ER stress in cardiomyocytes via miR-192-5p/SOD2 axis, suggesting the potential involvement of circ-SWT1 in AMI process.