LINC00511 accelerates the proliferation of cardiomyocytes after myocardial ischemia/reperfusion injury by absorbing miRNA-515-5p.

OBJECTIVE: The aim of this study was to clarify the role of LINC00511 in regulating the proliferative ability of cardiomyocytes undergoing ischemia/reperfusion (I/R) injury by absorbing miRNA-515-5p. MATERIALS AND METHODS: Adult male C57BL/6 mice were subjected to I/R injury, and I/R model was constructed in vivo. Primary cardiomyocytes were isolated from 1-2 days-old male mice and treated with H₂O₂ to establish the I/R model in vitro. The relative expression level of LINC00511 was determined after ligation of the anterior descending coronary artery (LAD) in mice or H₂O₂ induction in primary cardiomyocytes for different time points, respectively. The regulatory effect of LINC00511 on the viability of H₂O₂-treated cardiomyocytes was assessed. Subsequently, the interaction between LINC00511 and miRNA-515-5p was evaluated by Dual-Luciferase Reporter Gene Assay. Furthermore, the viability and 5-Ethynyl-2'-deoxyuridine (EdU)-positive rate influenced by LINC00511/miRNA-515-5p were examined. RESULTS: LINC00511 was gradually downregulated with the prolongation of I/R procedures in mice or H₂O₂ treatment in primary cardiomyocytes. The overexpression of LINC00511 significantly elevated the viability and EdU-positive rate in H₂O₂-treated cardiomyocytes. LINC00511 could bind to miRNA-515-5p. Meanwhile, there was a negative correlation between the levels of LINC00511 and miRNA-515-5p. In addition, the overexpression of miRNA-515-5p reversed the promoting effect of LINC00511 on the proliferative ability of H₂O₂-treated cardiomyocytes. CONCLUSIONS: LINC00511 accelerates the proliferation of cardiomyocytes after I/R by targeting miRNA-515-5p. [ABSTRACT FROM AUTHOR]