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Kv1.3 inhibition attenuates neuroinflammation through disruption of microglial calcium signaling
Channels ( IF 3.3 ) Pub Date : 2020-12-28 , DOI: 10.1080/19336950.2020.1853943
Alla F Fomina 1 , Hai M Nguyen 2 , Heike Wulff 2
Affiliation  

ABSTRACT

In the last 5 years inhibitors of the potassium channel KV1.3 have been shown to reduce neuroinflammation in rodent models of ischemic stroke, Alzheimer’s disease, Parkinson’s disease and traumatic brain injury. At the systemic level these beneficial actions are mediated by a reduction in microglia activation and a suppression of pro-inflammatory cytokine and nitric oxide production. However, the molecular mechanisms for the suppressive action of KV1.3 blockers on pro-inflammatory microglia functions was not known until our group recently demonstrated that KV1.3 channels not only regulate membrane potential, as would be expected of a voltage-gated potassium channel, but also play a crucial role in enabling microglia to resist depolarizations produced by the danger signal ATP thus regulating calcium influx through P2X4 receptors. We here review the role of KV1.3 in microglial signaling and show that, similarly to their role in T cells, KV1.3 channels also regulated store-operated calcium influx in microglia.



中文翻译:

Kv1.3抑制通过破坏小胶质细胞钙信号来减轻神经炎症

摘要

在过去的 5 年中,钾通道 K V 1.3 抑制剂已被证明可以减少缺血性中风、阿尔茨海默病、帕金森病和外伤性脑损伤的啮齿动物模型的神经炎症。在全身水平上,这些有益作用是通过减少小胶质细胞活化和抑制促炎细胞因子和一氧化氮产生来介导的。然而,直到我们小组最近证明K V1.3 通道不仅调节膜电位,正如电压门控钾通道所预期的那样,而且在使小胶质细胞能够抵抗由危险信号 ATP 产生的去极化从而通过 P2X4 受体调节钙内流方面发挥着至关重要的作用。我们在这里回顾了 K V 1.3 在小胶质细胞信号传导中的作用,并表明,与它们在 T 细胞中的作用类似,K V 1.3 通道也调节小胶质细胞中储存操作的钙流入。

更新日期:2020-12-28
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