Neuronal defect and loss are the main pathological processes of many central nervous system diseases. Cellular reprogramming is a promising method to supplement lost neurons. However, study on cellular reprogramming is still limited and its mechanism remains unclear. Herein, the effect of Neurod1 expression on differentiation of NG2 glia into neurons was investigated. In this study, we successfully isolated NG2 glial cells from mice prior to identification with immunofluorescence. Afterwards, AAV-Neurod1 virus was used to construct Neurod1 overexpression vectors in NG2 glia. Later, we detected neuronal markers expression with immunofluorescence and real time quantitative polymerase-chain reaction (qRT-PCR). Besides, expression of MAPK-signaling-pathway-related proteins were detected by western blotting technique. Through immunofluorescence and qRT-PCR techniques, we observed that Neurod1 overexpression contributed to NG2 cells differentiated into neurons. Further experiments also showed that Neurod1 overexpression induced the activation of MAPK pathway, but PD98059 (a selective inhibitor of MAPK pathway) partly inhibited the neuronal differentiation induced by Neurod1 overexpression. These findings suggest that Neurod1 could promote NG2 glia cells differentiating into neurons, wherein the mechanism under the differentiation is related to activation of MAPK pathway.

神经元缺损和丢失是许多中枢神经系统疾病的主要病理过程。细胞重编程是一种很有前途的方法来补充丢失的神经元。然而，对细胞重编程的研究仍然有限，其机制尚不清楚。在此，研究了 Neurod1 表达对 NG2 胶质细胞分化为神经元的影响。在这项研究中，我们成功地从小鼠中分离出 NG2 神经胶质细胞，然后用免疫荧光进行鉴定。随后，AAV-Neurod1 病毒用于在 NG2 胶质细胞中构建 Neurod1 过表达载体。后来，我们用免疫荧光和实时定量聚合酶链反应 (qRT-PCR) 检测了神经元标记物的表达。此外，通过蛋白质印迹技术检测MAPK信号通路相关蛋白的表达。通过免疫荧光和 qRT-PCR 技术，我们观察到 Neurod1 过表达有助于 NG2 细胞分化为神经元。进一步的实验还表明，Neurod1 过表达诱导了 MAPK 通路的激活，但 PD98059（MAPK 通路的选择性抑制剂）部分抑制了 Neurod1 过表达诱导的神经元分化。这些发现表明Neurod1可以促进NG2神经胶质细胞分化为神经元，其中分化机制与MAPK通路的激活有关。但 PD98059（MAPK 通路的选择性抑制剂）部分抑制了 Neurod1 过表达诱导的神经元分化。这些发现表明Neurod1可以促进NG2神经胶质细胞分化为神经元，其中分化机制与MAPK通路的激活有关。但 PD98059（MAPK 通路的选择性抑制剂）部分抑制了 Neurod1 过表达诱导的神经元分化。这些发现表明Neurod1可以促进NG2神经胶质细胞分化为神经元，其中分化机制与MAPK通路的激活有关。