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

There 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 Aβ(25-35) in...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6816367/
https://www.ncbi.nlm.nih.gov/pubmed/31564203
http://dx.doi.org/10.1080/15384101.2019.1669388
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author 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
author_facet 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
author_sort Zeng, Zhilei
collection PubMed
description There 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 Aβ(25-35) into 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 vivo of 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.
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spelling pubmed-68163672020-09-29 MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6 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 Cell Cycle Research Paper There 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 Aβ(25-35) into 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 vivo of 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. Taylor & Francis 2019-09-29 /pmc/articles/PMC6816367/ /pubmed/31564203 http://dx.doi.org/10.1080/15384101.2019.1669388 Text en © 2019 Informa UK Limited, trading as Taylor & Francis Group
spellingShingle Research Paper
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
MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6
title MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6
title_full MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6
title_fullStr MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6
title_full_unstemmed MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6
title_short MicroRNA-129-5p alleviates nerve injury and inflammatory response of Alzheimer’s disease via downregulating SOX6
title_sort microrna-129-5p alleviates nerve injury and inflammatory response of alzheimer’s disease via downregulating sox6
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6816367/
https://www.ncbi.nlm.nih.gov/pubmed/31564203
http://dx.doi.org/10.1080/15384101.2019.1669388
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