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论著:蛋白激酶C在肝细胞生长因子诱导血管内皮生长因子表达过程中的作用
Role of Protein Kinase C in the Process of Hepatocyte Growth Factor inducing Vascular Endothelial Growth Factor in MHCC97H
潘志刚 刘康达 胡美玉 吴伟忠
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作者单位:复旦大学附属中山医院全科医学科
中文关键字:肝细胞癌;蛋白激酶C;肝细胞生长因子;血管内皮生长因子
英文关键字:Hepatocellular carcinoma;Hepatocyte growth factor;Vascular endothelial growth factor;Protein kinase C
中文摘要:目的:探讨MHCC97H细胞中蛋白激酶C(PKCs)在肝细胞生长因子(hepatocyte growth factor,HGF)诱导血管内皮生长因子(vascular endothelial growth factor ,VEGF)表达过程中的作用。方法:将MHCC97H细胞分为对照组、HGF组、calphostin C组、BIM组、Ro31-8220组、ξ-PS 组,分别用逆转录聚合酶链反应(RT-PCR)、蛋白免疫印迹(Western Blot)法及免疫沉淀法分析各组中VEGF mRNA、蛋白质表达及磷酸化PKCξ水平变化情况。结果:广谱PKC抑制剂Ro31-8220能够完全抑制HGF所诱导的VEGF蛋白质升高(P<0.01)。calphostin C、BIM能够抑制HGF诱导的PKCβ和PKCδ磷酸化(均P<0.01)。BIM不能抑制HGF诱导的VEGF RNA及相应蛋白质的表达(P>0.05)。PKCζ特异性抑制蛋白ζ-PS能够抑制HGF诱导的PKCζ磷酸化及VEGF蛋白质表达(P<0.01)。结论:PKCs是MHCC97H细胞中HGF诱导VEGF表达路径的中间信号调节分子,HGF在MHCC97H细胞中主要通过磷酸化方式调节PKCs。HGF诱导的MHCC97H细胞的VEGF表达是通过aPKC的PKCξ调节的,cPKC、nPKC路径不参与MHCC97H中HGF诱导VEGF的表达过程。
英文摘要:Objective: To study the role of protein kinase C(PKCs) in the process of hepatocyte growth factor(HGF) inducing vascular endothelial growth factor(VEGF) in MHCC97H cells. Methods: MHCC97H cell line were cultured and divided into 6 groups: control group that without any additional stimuli; HGF group that added HGF at 60 ng/ml; calphostin C group that MHCC97H was cultured with calphostin C at 1μM 1h in advance and then added HGF at 60 ng/ml. BIM group that added BIM at 1μM 1h in advance and then added HGF at 60 ng/ml, Ro31-8220 group that cell was cultured with Ro31-8220 at 10μM 1h in advance and then added HGF at 60 ng/ml,ξ-PS group that added ξ-PS at 100μM 1h in advance and then added HGF at 60 ng/ml. RT-PCR,Western Blot and Immunoprecipitation were applied to analysis the expression of VEGF mRNA, VEGF protein, PKCs and phosphorylated PKCs, respectively. Results: In Ro31-8220 group, Ro31-8220 can totally blocked HGF-induced increasing expression of VEGF protein. Calphostin C and BIM can suppressed HGF-induced phosphorylation of PKCβ,PKCδ in MHCC97H respectively. BIM can not inhibited HGF-induced increasing expression of VEGF mRNA and protein. In ζ-PS group, ζ-PS can inhibited the phosphorylation of PKCξ and the expression of VEGF protein induced by HGF in MHCC97H, P<0.01 respectively. Conclusions: PKCs is signals in the pathway of VEGF expression induced by HGF. HGF can regulated phosphorylation of PKCs. The expression of VEGF induced by HGF is regulated by phosphorylatd PKCξ, and the pathway of cPKC and nPKC do not involved in this process.
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