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Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss
The contribution of the inwardly rectifying K(+) channel subtype Kir4.1 has been focused mainly on astrocytes, where they play important roles in the maintenance of resting membrane potential, extracellular K(+) uptake, and facilitation of glutamate uptake in the central nervous system. Here, we rep...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6123808/ https://www.ncbi.nlm.nih.gov/pubmed/30271961 http://dx.doi.org/10.1038/s42003-018-0083-x |
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author | Song, Feier Hong, Xiaoqi Cao, Jiayu Ma, Guofen Han, Yanfei Cepeda, Carlos Kang, Zizhen Xu, Tianle Duan, Shumin Wan, Jieqing Tong, Xiaoping |
author_facet | Song, Feier Hong, Xiaoqi Cao, Jiayu Ma, Guofen Han, Yanfei Cepeda, Carlos Kang, Zizhen Xu, Tianle Duan, Shumin Wan, Jieqing Tong, Xiaoping |
author_sort | Song, Feier |
collection | PubMed |
description | The contribution of the inwardly rectifying K(+) channel subtype Kir4.1 has been focused mainly on astrocytes, where they play important roles in the maintenance of resting membrane potential, extracellular K(+) uptake, and facilitation of glutamate uptake in the central nervous system. Here, we report the role of Kir4.1 channels in NG2-glia during brain development, potassium signaling, and in an ischemic stroke disease model. Kir4.1 channels are widely expressed in NG2-glia during brain development. In the adult mouse hippocampus, Kir4.1 channels in NG2-glia constitute more than 80% of K(+) channels inward currents. This large portion of Kir4.1 channel currents exhibits a deficit in NG2-glia as an initial response in a transient ischemic mouse model. Further evidence indicates that Kir4.1 deficits in NG2-glia potentially cause axonal myelin loss in ischemia through the association with oligodendrocyte-specific protein (OSP/Claudin-11), which unravels a potential therapeutic target in the treatment of ischemic stroke. |
format | Online Article Text |
id | pubmed-6123808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-61238082018-09-28 Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss Song, Feier Hong, Xiaoqi Cao, Jiayu Ma, Guofen Han, Yanfei Cepeda, Carlos Kang, Zizhen Xu, Tianle Duan, Shumin Wan, Jieqing Tong, Xiaoping Commun Biol Article The contribution of the inwardly rectifying K(+) channel subtype Kir4.1 has been focused mainly on astrocytes, where they play important roles in the maintenance of resting membrane potential, extracellular K(+) uptake, and facilitation of glutamate uptake in the central nervous system. Here, we report the role of Kir4.1 channels in NG2-glia during brain development, potassium signaling, and in an ischemic stroke disease model. Kir4.1 channels are widely expressed in NG2-glia during brain development. In the adult mouse hippocampus, Kir4.1 channels in NG2-glia constitute more than 80% of K(+) channels inward currents. This large portion of Kir4.1 channel currents exhibits a deficit in NG2-glia as an initial response in a transient ischemic mouse model. Further evidence indicates that Kir4.1 deficits in NG2-glia potentially cause axonal myelin loss in ischemia through the association with oligodendrocyte-specific protein (OSP/Claudin-11), which unravels a potential therapeutic target in the treatment of ischemic stroke. Nature Publishing Group UK 2018-06-28 /pmc/articles/PMC6123808/ /pubmed/30271961 http://dx.doi.org/10.1038/s42003-018-0083-x Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Song, Feier Hong, Xiaoqi Cao, Jiayu Ma, Guofen Han, Yanfei Cepeda, Carlos Kang, Zizhen Xu, Tianle Duan, Shumin Wan, Jieqing Tong, Xiaoping Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
title | Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
title_full | Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
title_fullStr | Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
title_full_unstemmed | Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
title_short | Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
title_sort | kir4.1 channels in ng2-glia play a role in development, potassium signaling, and ischemia-related myelin loss |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6123808/ https://www.ncbi.nlm.nih.gov/pubmed/30271961 http://dx.doi.org/10.1038/s42003-018-0083-x |
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