Long non‐coding RNA SENCR alleviates hypoxia/reoxygenation‐induced cardiomyocyte apoptosis and inflammatory response by sponging miR‐1

Background Myocardial cell apoptosis is one of the main reasons for the occurrence of acute myocardial infarction (AMI). The role of smooth muscle and endothelial cell enriched migration/differentiation-associated lncRNA (SENCR) in the cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) injury and its potential mechanism were investigated in this study to provide a novel biomarker for the development of AMI. Methods The expression levels of SENCR in the serum of AMI patients and non-AMI patients with chest pain (control) were detected by qRT-PCR. The function of SENCR in the cardiomyocyte apoptosis and inflammatory response induced by H/R injury was evaluated by MTT, cell apoptosis, and ELISA assay, respectively. The mechanism underlying the function of SENCR was investigated with the luciferase reporter assay. Results SENCR was significantly downregulated in AMI compared with the control volunteers, which showed negative correlations with the cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) level of patients. The H/R injury-induced cell apoptosis and inflammatory response in cardiomyocytes, which were attenuated by the overexpression of SENCR. The expression of miR-1 was suppressed by the overexpression of SENCR, while the overexpression of miR-1 could alleviate the cell apoptosis, enhance cell viability, and attenuate inflammatory response in cardiomyocyte. SENCR reversed H/R-induced myocardial cell injury by regulating the expression of miR-1. Conclusions SENCR was correlated with the clinicopathological features of patients and was revealed to alleviate the cardiomyocyte apoptosis and inflammatory response induced by H/R injury via sponging miR-1.