Department of Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany; Department of Neurology, University of Regensburg, Regensburg, Germany.
Department of Neurology, University Hospital Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
J Neuroimmunol. 2020 Jun 15;343:577227. doi: 10.1016/j.jneuroim.2020.577227. Epub 2020 Mar 24.
During neuroinflammation, the shaker type potassium channel Kv1.4 is re-expressed in oligodendrocytes (Ol), but not immune cells. Here, we analyze the role of endogenous Kv1.4 in two demyelinating animal models of multiple sclerosis. While Kv1.4 deficiency in primary murine Ol led to a decreased proliferation rate in vitro, it did not exert an effect on Ol proliferation or on the extent of de- or remyelination in the cuprizone model in vivo. However, in experimental autoimmune encephalomyelitis, Kv1.4 mice exhibited a milder disease course and reduced Th1 responses. These data argue for an indirect effect of Kv1.4 on immune cells, possibly via glial cells.
在神经炎症过程中，震颤型钾通道 Kv1.4 在少突胶质细胞（Ol）中重新表达，但不在免疫细胞中。在这里，我们分析了内源性 Kv1.4 在两种多发性硬化症的脱髓鞘动物模型中的作用。虽然初级鼠 Ol 中的 Kv1.4 缺乏导致体外增殖率降低，但它对 Ol 增殖或杯状内溶物模型中的脱髓鞘或再髓鞘程度没有影响。然而，在实验性自身免疫性脑脊髓炎中，Kv1.4 小鼠表现出较轻的疾病过程和减少的 Th1 反应。这些数据表明 Kv1.4 对免疫细胞有间接影响，可能通过神经胶质细胞。
