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

Abstract

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.