Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss.
Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss.
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NG2-神经胶质细胞中的 Kir4.1 通道在发育、钾信号传导和缺血相关髓磷脂丢失中发挥作用
DOI：
10.1038/s42003-018-0083-x
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发表时间：
2018
影响因子：
5.9
通讯作者：
Tong X
中科院分区：
文献类型：
--
作者：
Song F;Hong X;Cao J;Ma G;Han Y;Cepeda C;Kang Z;Xu T;Duan S;Wan J;Tong X
内向整流K+通道亚型Kir4.1的贡献主要集中在星形胶质细胞上，它们在维持静息膜电位、细胞外K+摄取和促进中枢神经系统中谷氨酸摄取方面发挥重要作用。在这里，我们报告的作用，Kir4.1通道在NG 2-胶质细胞在大脑发育，钾信号，并在缺血性中风疾病模型。Kir4.1通道在脑发育过程中广泛表达于NG 2-胶质细胞。在成年小鼠海马中，NG 2-胶质细胞中的Kir4.1通道占K+通道内向电流的80%以上。这一大部分Kir4.1通道电流在短暂性缺血小鼠模型中作为初始反应在NG 2-胶质细胞中表现出缺陷。进一步的证据表明，NG 2-胶质细胞中Kir4.1缺陷可能通过与少突胶质细胞特异性蛋白（OSP/Claudin-11）的相关性导致缺血中轴突髓鞘丢失，这揭示了治疗缺血性卒中的潜在治疗靶点。
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.