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作 者:朱萍[1] 冯吉[2] 杨荟敏[1] 谷利[1] 张红[1]
机构地区:[1]首都医科大学细胞生物学系,北京100069 [2]首都医科大学化学生物学与药学院,北京100069
出 处:《中国生物化学与分子生物学报》2010年第4期332-340,共9页Chinese Journal of Biochemistry and Molecular Biology
基 金:国家自然基金资助项目(No.30873087);北京自然基金资助项目(No.7082010);北京市教委资助项目(No.KM200910025001);北京市属高等学校人才强教计划资助项目(IHLB)~~
摘 要:血清因子能调节细胞的生长与凋亡,但是其分子机制尚不清楚.通过细胞培养基中血清存在与否,研究了代谢型谷氨酸受体1(mGluR1)介导的胞外信号调节激酶(ERK),蛋白激酶B(PKB/AKT)通路的活化及其对细胞生长与凋亡的影响.在过量表达mGluR1的HEK293细胞中,血清饥饿促进了mGluR1对ERK,AKT信号通路的活化;细胞凋亡剂STS应激损伤时,受体激动剂DHPG可降低细胞活性,促进细胞凋亡.在大鼠胶质瘤细胞中,与过表达mGluR1的HEK293细胞的结果相反,血清有助于mGluR1对ERK,AKT通路的活化作用;STS应激损伤时,内源性mGluR1的活化抑制了细胞凋亡.结果表明:血清中存在的细胞因子,通过细胞中表达水平不同的mGluR1受体,调节受体介导的信号通路,从而调控细胞生长与凋亡.本文可能揭示了一种血清调节细胞生长与凋亡的新机制.The mechanism of serum to regulate cell growth and apoptosis remained unclear.We investigated whether it is involved the metabotropic glutamate receptor 1(mGluR1)-mediated extracellular signal-regulated kinase(ERK) and protein kinase(PKB /AKT) pathways.In mGluR1-overexpressing HEK293 cells,the activation of ERK and AKT pathways was promoted with the serum withdrawal.The treatment of mGluR1 agonist STS(Staurosporine) or DHPG induced apoptosis and reduced the cell viability.Whereas in C6 rat glial cells,the activation of ERK and AKT pathways mediated by endogenous mGluR1 was enhanced at the presence of serum,and the cells were resistant toSTS-induced apoptosis.Our data suggested that the different expression levels in of mGluR1 in HEK293 cells and C6 cells might contribute to the serum responses in cell growth and STS-induced apoptosis.
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