Abstract：
The functions of Kir4.1 in oligodendrocyte development have been in controversial. We recently reported that inhibiting Kir4.1 impeded oligodendrocyte precursor cell (OPC) differentiation and oligodendrocyte (OL) maturation, due to Kir4.1 altering intracellular pH of OPCs through Na+/H+ exchangers. However, our conclusion was limited by in vitro observation, thereby it becomes necessary to seek in vivo evidence to determine the roles of Kir4.1 on OPC development and CNS myelination. Here, we used Olig1-Cre to knockout Kir4.1 in OPCs from the early developmental stage. We found that the cell-specific deletion of Kir4.1 significantly impeded OPC differentiation and reduced the number of mature OLs in the cerebral cortex and the corpus callosum. Hence, our in vivo evidence supports that Kir4.1 can regulate OPC differentiation and is essential to CNS myelination.
摘要：
Kir4.1在少突胶质细胞发育中的功能一直存在争议。我们最近报道，抑制Kir4.1阻碍少突胶质细胞前体细胞（OPC）分化和少突胶质细胞（OL）成熟，由于Kir4.1通过Na+/H+交换剂改变OPCs的细胞内pH。然而,我们的结论受到体外观察的限制，因此，有必要寻找体内证据来确定Kir4.1对OPC发育和CNS髓鞘形成的作用。这里,我们使用Olig1-Cre从早期发育阶段敲除OPCs中的Kir4.1。我们发现Kir4.1的细胞特异性缺失显着阻碍了OPC的分化，并减少了大脑皮层和call体的成熟OLs的数量。因此，我们的体内证据支持Kir4.1可以调节OPC分化,并且对CNS髓鞘形成至关重要.
