文献类型：期刊文献

英文题名：miR-126-5p Targets SP1 to Inhibit the Progression of Parkinson's Disease

作者：Han, Yan-Ping[1];Liu, Zhi-Jun[1];Bao, Hong-Hui[1];Wang, Qiong[1];Su, Li-Li[1]

第一作者：韩艳萍

通信作者：Han, YP[1]

机构：[1]Gansu Univ Chinese Med, Dept Neurol, Affiliated Hosp, Lanzhou, Peoples R China

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Dept Neurol, Affiliated Hosp, Lanzhou, Peoples R China.|[10735b845793de6ae2b30]甘肃中医药大学第二附属医院;[10735]甘肃中医药大学;

年份：2022

卷号：85

期号：3

起止页码：235

外文期刊名：EUROPEAN NEUROLOGY

收录：;Scopus(收录号：2-s2.0-85124630260);WOS:【SCI-EXPANDED(收录号:WOS:000750625100001)】；

语种：英文

外文关键词：Parkinson' disease; miR-126-5p; Specific protein-1; 1-Methyl-4-phenylpyridinium

摘要：Background: At present, symptomatic treatment may improve the life quality of Parkinson's disease (PD) patients to a certain extent but cannot completely cure PD. Therefore, it is urgent medical problem to be solved for improving the efficacy and safety of PD treatment. Methods: SH-SY5Y and SK-N-SH cells were treated with 1-methyl-4-phenylpyridinium (MPP+) to establish PD model cells. miR-126-5p and specific protein-1 (SP1) expression levels were detected by quantitative Real-Time PCR (qRT-PCR). Western blot was applied to measure protein levels of SP1, Bax, and Bcl-2. The viabilities and apoptosis rates of treated cells were measured using cell counting kit-8 assay and flow cytometry analysis. Enzyme-linked immunosorbent assay was performed to measure TNF-alpha and IL-1 beta releases. Interaction between miR-126-5p and SP1 was examined by dual-luciferase reporter assay. Results: MPP+ treatment greatly downregulated miR-126-5p expression while upregulated SP1 expression in SH-SY5Y and SK-N-SH cells in a time- and does-dependent manner. Overexpression of miR-126-5p facilitated cell viability, while reduced cell apoptosis and inflammatory responses induced by MPP+ treatment. Moreover, SP1 was a target of miR-126-5p and could be negatively regulated by miR-126-5p. Overexpression of SP1 could reverse the effects of miR-126-5p on MPP+-administrated cells. Conclusion: Our results suggested that miR-126-5p attenuated the neurotoxicity induced by MPP+ in vitro through targeting SP1 (Graphical abstract), which further enhanced our understanding of the pathological mechanism of PD.