Abstract

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.

摘要

目前治疗心肌梗死最有效的方法是再灌注，再灌注不可避免地导致心肌细胞凋亡。在本研究中，我们讨论了 SNHG15 通过调节 miR-188-5p/PTEN 轴调节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、western blotting、荧光素酶报告分析、流式细胞术分析等。通过一系列的比较和分析，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学。PTEN 在缺氧细胞中上调，但这种效应被 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 MCs 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。