SNHG16 accelerates the proliferation of primary cardiomyocytes by targeting miRNA7705p

The present study aimed to clarify the influence of long noncoding 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 H2O2 treatment to mimic in vitro IRI. Relative levels of SNHG16 and miRNA7705p in both in vivo and in vitro IRI models were examined. The regulatory effects of SNHG16 and miRNA7705p on the proliferative ability of H2O2treated cardiomyocytes were assessed by Cell Counting Kit8 (CCK8) and 5ethynyl2'deoxyuridine (EdU) assay. The binding relationship between SNHG16 and miRNA7705p was verified through dualluciferase reporter gene assay. It is found that SNHG16 was timedependently downregulated in the IRI models. Overexpression of SNHG16 enhanced the proliferative ability of the cardiomyocytes. miRNA7705p was found to be a direct target of SNHG16. Moreover, SNHG16 was able to negatively regulate the miRNA7705p level. Overexpression of miRNA7705p partially reversed the role of SNHG16 on accelerating cardiomyocyte proliferation. Collectively, SNHG16 accelerates the proliferative ability of cardiomyocytes following IRI by negatively regulating miRNA7705p.