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机构地区:[1]中国医科大学基础医学院生物信息学教研室,辽宁沈阳110001
出 处:《中华肿瘤防治杂志》2007年第9期660-661,685,共3页Chinese Journal of Cancer Prevention and Treatment
摘 要:目的:研究Caveolin-1蛋白在内皮细胞增殖中的作用,其与Ras-p42/44MAPK细胞信号通路的关系。方法:以腺病毒介导在内皮细胞中表达外源Caveolin-1蛋白,分析其对内皮细胞增殖和p42/44MAPK分子磷酸化水平的影响。结果:感染腺病毒表达外源Caveolin-1蛋白的内皮细胞中,血管内皮生长因子(VEGF)诱导的3H-胸腺嘧啶掺入量降低了35%(n=3,P=0.009),p42/44MAPK分子磷酸化水平降低了47.6%。结论:Caveolin-1蛋白抑制p42/44MAPK分子磷酸化水平,抑制内皮细胞增殖。OBJECTIVE: To investigate the effect of cave olin-1 on the endothelial cell proliferation and the molecular mechanism. METHODS: The adenovirus as a vector was ex ployed to express the exogenous caveolin-1 protein, the prolifer ation by was determined 3 H-thymidine incorporation assay, and the activity of p42/44MAPK was determined by Western blot. RESULTS: The incorporation of 3H-thymidine induced by VEGF was decreased by 35 % (n = 3, P = 0. 009) in endothelial cells, and the phosphorylation level of p42/44MAPK was decreased by 47.60%. CONCLUSION: Caveolin-1 inhibits the phosphorylation level of p42/44MAPK and the proliferation of endothelial cells.
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