Nowadays the most effective way to cure myocardial infarction (MI) is reperfusion, which inevitably leads to cardiomyocyte apoptosis. In this study, we discussed the functions of SNHG15 in regulating cardiomyocyte apoptosis through the modulation of miR-188-5p/PTEN axis. We examined the links between SNHG15 and miR-188-5p/PTEN in mice with MI. Extensive experiments, measurements and comparisons were performed, including RT-PCR, western blotting, luciferase reporter assay, flow cytometry analysis etc. Through a series of comparisons and analysis, we discovered that SNHG15 could interact with the miR-188-5p/PTEN axis and impact the cellular physiology of cardiomyocyte apoptosis. PTEN was upregulated in hypoxia cells, but this effect was attenuated by miR-188-5p. MiR-188-5p could combine with SNHG15 and PTEN, and form a SNHG15-miR-188-5p-PTEN axis, which regulated the apoptosis of MCs. These results suggest that LncRNA SNHG15 regulates cardiomyocyte apoptosis induced by hypoxia or reperfusion injury through modulating of miR-188-5p/PTEN axis.

如今，治疗心肌梗塞（MI）的最有效方法是再灌注，这不可避免地导致心肌细胞凋亡。在这项研究中，我们讨论了SNHG15通过调节miR-188-5p / PTEN轴调控心肌细胞凋亡的功能。我们检查了MI小鼠中SNHG15和miR-188-5p / PTEN之间的联系。进行了广泛的实验，测量和比较，包括RT-PCR，蛋白质印迹，荧光素酶报告基因分析，流式细胞仪分析等。通过一系列比较和分析，我们发现SNHG15可以与miR-188-5p / PTEN轴相互作用并影响心肌细胞凋亡的细胞生理。PTEN在缺氧细胞中上调，但这种作用被miR-188-5p减弱。MiR-188-5p可以与SNHG15和PTEN结合，形成SNHG15-miR-188-5p-PTEN轴，调节MC的凋亡。这些结果表明，LncRNA SNHG15通过调节miR-188-5p / PTEN轴来调节缺氧或再灌注损伤诱导的心肌细胞凋亡。