LncRNA RMRP accelerates hypoxia-induced injury by targeting miR-214-5p in H9c2 cells

Abstract Objective To elucidate the function of lncRNA RMRP in hypoxia-induced acute myocardial infarction (AMI) in vitro and explore its underlying mechanism. Methods Hypoxic injury was confirmed by measurement of cell viability, LDH release, migration, invasion, and apoptosis in H9c2 cells. The interactions between RMRP and miR-214-5p as well as miR-214-5p and p53 were also investigated. Results Hypoxia treatment significantly induced cell damage in H9c2 cells, accompanied with the up-regulation of RMRP expressions. Transfection of RMRP siRNA remarkably attenuated hypoxia-induced injury by enhancing cell viability, migration and invasion, and reducing cell apoptosis and LDH release; whereas, enforced expression of RMRP aggravated hypoxia-induced injury. Furthermore, RMRP served as an endogenous sponge for miR-214-5p, and its expression was negatively regulated by RMRP. The effects of RMRP knockdown on hypoxia-induced injury were further enhanced with miR-214-5p overexpression, but significantly abrogated with miR-214-5p silence. Moreover, p53 was verified as a direct target of miR-214-5p, and functional investigation revealed that RMRP regulated hypoxia-induced injury via modulating p53 signaling pathway, which was partially mediated by miR-214-5p. Conclusion Our findings demonstrated the novel molecular mechanism of RMRP/miR-214-5p/p53 axis on the regulation of hypoxia-induced myocardial injury in H9c2 cells, which might provide potential therapeutic targets for AMI treatment.