Deficiency of microglial Hv1 channel is associated with activation of autophagic pathway and ROS production in LPC-induced demyelination mouse model.
Deficiency of microglial Hv1 channel is associated with activation of autophagic pathway and ROS production in LPC-induced demyelination mouse model.
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LPC 诱导的脱髓鞘小鼠模型中小胶质细胞 Hv1 通道的缺陷与自噬途径的激活和 ROS 的产生有关
DOI：
10.1186/s12974-020-02020-y
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发表时间：
2020-11-06
影响因子：
9.3
通讯作者：
Tian DS
中科院分区：
文献类型：
--
作者：
Chen M;Yang LL;Hu ZW;Qin C;Zhou LQ;Duan YL;Bosco DB;Wu LJ;Zhan KB;Xu SB;Tian DS
Multiple sclerosis (MS) is an immune-mediated demyelinated disease of the central nervous system. Activation of microglia is involved in the pathogenesis of myelin loss. This study is focused on the role of Hv1 in regulating demyelination and microglial activation through reactive oxygen species (ROS) production after lysophosphatidylcholine (LPC)-mediated demyelination. We also explored autophagy in this process. A model of demyelination using two-point LPC injection into the corpus callosum was established. LFB staining, immunofluorescence, Western blot, and electron microscopy were used to study the severity of demyelination. Microglial phenotype and autophagy were detected by immunofluorescence and Western blot. Morris water maze was used to test spatial learning and memory ability. We have identified that LPC-mediated myelin damage was reduced by Hv1 deficiency. Furthermore, we found that ROS and autophagy of microglia increased in the demyelination region, which was also inhibited by Hv1 knockout. These results suggested that microglial Hv1 deficiency ameliorates demyelination through inhibition of ROS-mediated autophagy and microglial phenotypic transformation.
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小胶质细胞 Hv1 质子通道通过氧化损伤促进铜宗诱导的脱髓鞘。
影响因子：
4.7
作者：
Liu J;Tian D;Murugan M;Eyo UB;Dreyfus CF;Wang W;Wu LJ
通讯作者：
Wu LJ
DOI：
10.1093/brain/aws012
发表时间：
2012-03
期刊：
Brain : a journal of neurology
影响因子：
--
作者：
Fischer MT;Sharma R;Lim JL;Haider L;Frischer JM;Drexhage J;Mahad D;Bradl M;van Horssen J;Lassmann H
通讯作者：
Lassmann H
影响因子：
9.3
作者：
Chu, Tianci;Zhang, Yi Ping;Cai, Jun
通讯作者：
Cai, Jun
影响因子：
4.8
作者：
Pugsley, Haley R.
通讯作者：
Pugsley, Haley R.
影响因子：
13.3
作者：
Moore, Michael N.
通讯作者：
Moore, Michael N.