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.