LncRNA SENCR Ameliorates Hypoxia-Induced Myocardial Infarction by Targeting the miR-206/SMAD4 Axis

Abstract

Background: The long non-coding RNAs (lncRNAs) have been found crucial in the pathogenesis of cardiovascular diseases, including myocardial infarction (MI). Therefore, we aimed to investigate the role of lncRNA smooth muscle and endothelial cell-enriched migration/differentiation-associated lncRNA (SENCR) in MI. Methods: An in vitro model of MI was established by treating human cardiomyocytes (HCM) with hypoxia conditions. The quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analysis were used to assess the expression of genes both at RNA and protein levels. However, Cell Counting Kit-8 (CCK-8) and flow cytometry analysis were employed for the assessment of HCM viability and apoptosis. Furthermore, RNA-binding protein immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays were conducted to explore the regulatory relationship between SENCR and related molecules. Results: The expression levels of SENCR were found to be progressively reduced in HCM under hypoxia treatment (p < 0.01). Furthermore, overexpression of SENCR stimulated HCM viability and reduced apoptosis rate during hypoxia conditions (p < 0.01). Moreover, SENCR was found to function as a competing endogenous RNA (ceRNA) to sequester miR-206, consequently modulating SMAD family member 4 (SMAD4) expression (p < 0.01). Conclusions: LncRNA SENCR ameliorated hypoxia-induced MI by targeting the miR-206/SMAD4 axis. The findings of this research might offer novel insight for improving the treatment of MI.