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机构地区:[1]军事医学科学院基础医学研究所,北京100850
出 处:《中华微生物学和免疫学杂志》2002年第3期339-341,共3页Chinese Journal of Microbiology and Immunology
基 金:国家杰出青年科学基金资助项目 (3992 50 1 9)
摘 要:目的 研究IFN α在人骨髓瘤细胞系U2 6 6上的生物学效应及其分子机制。方法 采用MTT方法检测IFN α对U2 6 6细胞生长的影响 ;采用FACS方法检测IFN α作用下U2 6 6细胞生长周期及其表面IL 6R、gp130等分子表达水平的改变情况 ;采用免疫印迹方法检测能够介导细胞生长的Ras/MAPK途径中蛋白激酶ERK在IFN α刺激作用下的活化情况 ,并同时观察Ras/MAPK途径特异性抑制剂PD980 5 9作用后ERK激酶活化和细胞生长所发生的变化。结果 IFN α能够促进U2 6 6细胞周期行进 ,同时表现出细胞增殖促进效应 ;但它不影响U2 6 6细胞上IL 6R和gp130分子的表达。IFN α可明显激活蛋白激酶ERK ,PD980 5 9作用后ERK活化受抑 ,同时IFN α在U2 6 6细胞上的生长促进效应明显下调。结论 IFN α通过激活蛋白激酶ERK介导其在U2 6Objective To investigate the biological activity and molecular mechanism of IFN α on human myeloma cell line U266. Methods The effect of IFN α on the growth of U266 cells was measured by MTT assay; U266 cells cycle distribution and the expression of IL 6R and gp130 on the cell surface in the absence or presence of IFN α were monitored by FACS analysis. Immunoblot assay was used in U266 cells stimulated by IFN α to detect the activation of protein kinase ERK, that is involved in Ras/MAPK signal transduction pathway mediating cell survival and proliferation. Then the changes on U266 cells proliferation and ERK activation induced by IFN α were examined in the presence of PD98059, the specific antagonist of Ras/MAPK pathway. Results IFN α promoted cell cycle progression and proliferation of U266 cells, but it did not show any effect on the expression of IL 6R and gp130 on cell surface. ERK was activated in U266 cells stimulated by IFN α, but both cell proliferation and ERK activation were obviously inhibited in the presence of PD98059. Conclusion The proliferative effect of IFN α on U266 cells is mediated by activation of protein kinase ERK. [
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