SNHG16 accelerates the proliferation of primary cardiomyocytes by targeting miRNA-770-5p

The present study aimed to clarify the influence of long non-coding RNA small nuclear host gene 16 (lncRNA SNHG16) on cardiomyocyte proliferation following ischemia/reperfusion injury (IRI) and the potential mechanism. An IRI model in mice was established by performing ligation of the anterior descending coronary artery (LAD). Primary cardiomyocytes were isolated from newborn mice and subjected to H(2)O(2) treatment to mimic in vitro IRI. Relative levels of SNHG16 and miRNA-770-5p in both in vivo and in vitro IRI models were examined. The regulatory effects of SNHG16 and miRNA-770-5p on the proliferative ability of H(2)O(2)-treated cardiomyocytes were assessed by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assay. The binding relationship between SNHG16 and miRNA-770-5p was verified through dual-luciferase reporter gene assay. It is found that SNHG16 was time-dependently downregulated in the IRI models. Overexpression of SNHG16 enhanced the proliferative ability of the cardiomyocytes. miRNA-770-5p was found to be a direct target of SNHG16. Moreover, SNHG16 was able to negatively regulate the miRNA-770-5p level. Overexpression of miRNA-770-5p partially reversed the role of SNHG16 on accelerating cardiomyocyte proliferation. Collectively, SNHG16 accelerates the proliferative ability of cardiomyocytes following IRI by negatively regulating miRNA-770-5p.