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MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6

Authors :
Zeng, Zhilei
Liu, Yajun
Zheng, Wei
Liu, Liubin
Yin, Honglei
Zhang, Simiao
Bai, Hongying
Hua, Linlin
Wang, Shanshan
Wang, Zhen
Li, Xiaodong
Xiao, Jianhao
Yuan, Qian
Wang, Yunliang
Source :
Cell Cycle; November 2019, Vol. 18 Issue: 22 p3095-3110, 16p
Publication Year :
2019

Abstract

ABSTRACTThere is growing evidence of the position of microRNAs (miRs) in Alzheimer’s disease (AD), thus our objective was to discuss the impact of miR-129-5p regulating nerve injury and inflammatory response in AD rats by modulating SOX6 expression. The AD rat model was established by injecting Aβ25-35into the brain. The pathological changes, ultrastructure, number of neurons, cell degeneration and apoptosis of hippocampal tissue were observed in vivo. MiR-129-5p, SOX6, IL-1β, TNF-α, Bcl-2 and Bax expression in serum and hippocampal tissues were detected by ELISA, RT-qPCR or western blot analysis. The successfully modeled hippocampal neuronal cells of AD were transfected with miR-129-5p mimic, SOX6-siRNA or their controls to figure out their roles in proliferation, apoptosis and inflammatory reaction in vitro. Low expression of SOX6 and high expression of miR-129-5p in vivoof rats would shorten the escape latent period and increase the times of crossing platforms, alleviate the pathological injury, inhibit neuronal apoptosis and reduce the inflammatory reaction. Up-regulation of miR-129-5p and down-regulation of SOX6 promoted proliferation, suppressed apoptosis and degraded the inflammatory reaction of neuronal cells in vitro. Up-regulation of SOX6 reversed the expression of miR-129-5p to reduce the damage and inflammatory response of the cell model of AD. Our study presents that up-regulation of miR-129-5p or down-regulation of SOX6 can reduce nerve injury and inflammatory response in rats with AD. Thus, miR-129-5p may be a potential candidate for the treatment of AD.

Details

Language :
English
ISSN :
15384101 and 15514005
Volume :
18
Issue :
22
Database :
Supplemental Index
Journal :
Cell Cycle
Publication Type :
Periodical
Accession number :
ejs51320804
Full Text :
https://doi.org/10.1080/15384101.2019.1669388