长链非编码RNA RPSAP52通过调控miR-423-5p/GSTM1轴抑制缺氧诱导的肾近端小管上皮细胞凋亡。
LncRNA RPSAP52 regulates miR-423-5p/GSTM1 axis to suppress hypoxia-induced renal proximal tubular epithelial cell apoptosis.
作者信息
Chen Jie, Zheng Yu, Li Liping
机构信息
Injury Prevention Research Center, Shantou University Medical College, Shantou, P.R. China.
Department of Urology, The Second Affiliated Hospital of Shantou University Medical College, Shantou, P.R. China.
出版信息
Arch Physiol Biochem. 2022 Aug;128(4):1066-1070. doi: 10.1080/13813455.2020.1750657. Epub 2020 Apr 17.
This study aimed to investigate the roles of RPSAP52 in renal failure. Our results showed that RPSAP52 was upregulated in plasma of renal failure patients in comparison to healthy controls. Dual luciferase reporter assay showed that RPSAP52 could interact with miR-423-5p, while overexpression of RPSAP52 and miR-423-5p did not alter the expression of each other in human renal proximal tubular epithelial cells (HRPTEpCs). In addition, overexpression of RPSAP52 increased the expression levels of GSTM1 in HRPTEpCs. Cell apoptosis assay showed that overexpression of RPSAP52 and GSTM1 decreased the apoptotic rate of HRPTEpCs under hypoxia conditions. MiR-423-5p played an opposite role and attenuated the effects of overexpressing RPSAP52 and GSTM1. Therefore, RPSAP52 may regulate miR-423-5p/GSTM1 axis to suppress hypoxia-induced HRPTEpC apoptosis.
本研究旨在探讨RPSAP52在肾衰竭中的作用。我们的结果表明，与健康对照相比，RPSAP52在肾衰竭患者血浆中上调。双荧光素酶报告基因检测表明，RPSAP52可与miR-423-5p相互作用，而在人肾近端小管上皮细胞（HRPTEpCs）中，RPSAP52和miR-423-5p的过表达并未改变彼此的表达。此外，RPSAP52的过表达增加了HRPTEpCs中GSTM1的表达水平。细胞凋亡检测表明，RPSAP52和GSTM1的过表达降低了缺氧条件下HRPTEpCs的凋亡率。miR-423-5p发挥相反作用，并减弱了RPSAP52和GSTM1过表达的影响。因此，RPSAP52可能通过调节miR-423-5p/GSTM1轴来抑制缺氧诱导的HRPTEpC凋亡。
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