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MAPK、PI3K途径在蛇毒神经生长因子诱导PC12细胞分化的作用
引用本文:何艳,汪效英,陈崇宏.MAPK、PI3K途径在蛇毒神经生长因子诱导PC12细胞分化的作用[J].福建医科大学学报,2007,41(1):5-8.
作者姓名:何艳  汪效英  陈崇宏
作者单位:1. 福建医科大学,生化与分子生物学系,福州,350004
2. 福建医科大学,药学院,福州,350004
基金项目:福建省自然科学基金 , 福建医科大学教授基金
摘    要:目的 研究丝裂原激活蛋白激酶(MAPK)和磷脂酰肌醇3-激酶(PI3K)/Akt途径在蛇毒神经生长因子(NGF)诱导PC12细胞分化中的作用.方法 应用蛋白免疫印迹法分析p44/p42MAPK和Akt的磷酸化水平,并利用MAPK抑制剂PD98059和PI3K抑制剂LY294002,观察其对NGF诱导的PC12细胞形态学改变的影响.结果 眼镜蛇毒NGF在10ng/mL即可诱导PC12细胞长出突起,100,1000ng/mL作用明显,呈剂量效应关系;NGF能有效刺激p44/p42MAPK、Akt的磷酸化;分别用特异抑制剂PD98059抑制MAPK活性,LY294002抑制PI3K活性后,NGF诱导的细胞分化均受抑制.结论 蛇毒神经生长因子诱导PC12细胞的分化作用与p44/p42MAPK和PI3K/Akt途径相关.

关 键 词:神经生长因子  PC12细胞  细胞分化  信号传导
文章编号:1672-4194(2007)01-0005-04
修稿时间:2006-10-27

Role of MAPK and PI3K in Nerve Growth Factor-Induced Differentiation of PC12
He Yan,Wang Xiaoying,Chen Chonghong.Role of MAPK and PI3K in Nerve Growth Factor-Induced Differentiation of PC12[J].Journal of Fujian Medical University,2007,41(1):5-8.
Authors:He Yan  Wang Xiaoying  Chen Chonghong
Institution:1. Division of Biochemistry and Molecular Biology; 2. College of Pharmacy, Fujian Medical University, Fuzhou 350004, China
Abstract:Objective To investigate the role of mitogen-activated protein kinase(MAPK) and phosphoinositide 3-kinase(PI3K)/Akt pathways in differentiation of PC12 cells induced by nerve growth factor(NGF) from venom.Methods The phosphorylation of p44/p42MAPK and Akt were detected by Western blot.The role of MAPK and PI3K in the cellular action of PVC12 cells induced by NGF were assessed by use MAPK and PI3K specific inhibitor PD98059 and LY294002 respectively.Results NGF from cobra venom can stimulate p44/p42MAPK and Akt phosphorylation and induce the differentiation of PC12 cells from 10 ng/mL~()to 1000 ng/mL.The differentiation of PC12 cells induced by NGF was inhibited when MAPK or PI3K pathway was abolished by the specific inhibitor PD98059 and LY294002.(Conclusion) The differentiation of PC12 cells by NGF from cobra venom relates to p44/p42MAPK and PI3K/Akt pathway.
Keywords:nerve growth factor  PC12 cell  cell differentiation  signal transduction
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