Erk信号途径在B104 CM诱导神经干细胞向少突胶质细胞前体分化中的作用  

THE ROLE OF Erk SIGNAL PATHWAY IN B104 CM-INDUCED OPC DIFFERENTIATION FROM NSCs

作　　者：胡建国[1] 钟政荣[1] 王凤超[1] 富赛里[2] 陆佩华[2] 

机构地区：[1]蚌埠医学院附属医院检验科,蚌埠233004 [2]上海交通大学医学院神经生物学实验室,上海200025

出　　处：《解剖学报》2008年第2期155-159,共5页Acta Anatomica Sinica

基　　金：安徽省教育厅自然科学基金重点项目(2006KJ098A)资助

摘　　要：目的探讨细胞外信号调节激酶(Erk)信号途径及下游转录因子cf-os、cj-un等在神经母细胞瘤B104细胞系来源的条件培养基(B104 CM)诱导神经干细胞(NSCs)向少突胶质细胞前体(OPCs)分化中的作用。方法从形态学上观察Erk1/2特异性抑制剂U0126阻断对B104 CM诱导NSCs向OPCs分化的影响;分别以Western blotting和RT-PCR法检测对照组、B104 CM诱导组和U0126预孵组NSCs中Erk的磷酸化和转录因子cf-os、cj-un、c-myc的表达情况。结果U0126预孵可阻断B104 CM诱导的NSCs向OPCs分化;B104 CM可引起NSCs中Erk1/2迅速磷酸化和cf-os、cj-unmRNA表达上调,该作用可被U0126阻断。结论B104 CM通过活化Erk信号途径及其随后上调转录因子cf-os、cj-un的表达诱导NSCs向OPCs分化。Objective To investigate the role of extracellular signal-regulated kinase（Erk） and transcriptional factors such as c-fos,c-jun in B104 CM-induced oligodendrocyte progenitor cells（OPCs） differentiation from neural stem cells（NSCs）.Methods The effect of U0126,the specific inhibitor of Erk1/2,on B104 CM-induced OPC differentiation from NSCs was observed by morphology.The phosphorylation of Erk1/2 and mRNA expression of transcriptional factors c-fos,c-jun and c-myc in NSCs in the control group,B104 CM-treated group and U0126 pre-incubated group were detected by Western blotting and RT-PCR methods respectively.Results B104 CM-induced OPC differentiation from NSCs could be blocked by pre-incubation of U0126.Treatment of NSCs with B104 CM produced a rapid increase in phosphorylation of Erk1/2 and an upregulation of c-fos and c-jun mRNA expression,which could be blocked by the pre-incubation of U0126.Conclusion B104 CM instructs oligodendrocyte differentiation from NSCs through the activation of Erk1/2 signal pathway and sequential upregulation of the expression of transcriptional factors c-fos and c-jun.

关 键 词：神经母细胞瘤B104细胞系来源的条件培养基 神经干细胞 少突胶质细胞前体 分化 细胞外信号调节激酶 免疫印迹法 逆转录聚合酶链反应 大鼠 

分 类 号：Q512[生物学—生物化学]