Chen Dapeng, Zhang Zhengjun, Lu Xiaorui, Yang Xinbin
Heart Center, General Hospital of Ningxia Medical University, Yinchuan, PR China.
Department of Internal Medicine-Cardiovascular, Ningxia Yongning County People's Hospital, Ningxia, PR China.
Arch Physiol Biochem. 2023 Apr;129(2):283-290. doi: 10.1080/13813455.2020.1819336. Epub 2020 Sep 24.
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.
目前,治疗心肌梗死(MI)最有效的方法是再灌注,而这不可避免地会导致心肌细胞凋亡。在本研究中,我们探讨了SNHG15通过调节miR-188-5p/PTEN轴在调控心肌细胞凋亡中的作用。我们研究了MI小鼠中SNHG15与miR-188-5p/PTEN之间的联系。进行了广泛的实验、测量和比较,包括逆转录聚合酶链反应(RT-PCR)、蛋白质免疫印迹法、荧光素酶报告基因检测、流式细胞术分析等。通过一系列比较和分析,我们发现SNHG15可与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,但这种作用被miR-188-5p减弱。miR-188-5p可与SNHG15和PTEN结合,形成SNHG15-miR-188-5p-PTEN轴,该轴调节心肌细胞的凋亡。这些结果表明,长链非编码RNA SNHG15通过调节miR-188-5p/PTEN轴来调控缺氧或再灌注损伤诱导的心肌细胞凋亡。