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《Chinese Journal of Pathophysiology》 2011-12
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LPS induced B7-H1 expression in pancreatic carcinoma Panc-1 cells

MA Jun1,2,HUANG Dong-sheng1,JIN Hong-chuan3,LIU Jun-wei1,SHEN Guo-liang1,WANG Fan1(1Department of General Surgery,2Key Laboratory of Biotherapy of Zhejiang Province,3Biomedical Research Center,the Affiliated Sir Run Run Shaw Hospital,Zhejiang University School of Medicine,Hangzhou 310016,China)  
AIM: To explore the mechanism of lipopolysaccharide(LPS)-induced B7-H1 expression in pancreatic carcinoma cell line Panc-1.METHODS: The levels of phosphorylated p38 mitogen-activated protein kinase(p-p38),phosphorylated extracellular signal-regulated kinase(p-ERK) and phosphorylated c-Jun N-terminal kinase(p-JNK) after stimulated with LPS or treated with mitogen-activated protein kinases(MAPKs) inhibitors were detected by Western blotting.The expression of B7-H1 in Panc-1 cells after LPS stimulation or MAPKs inhibitor treatment was measured by real-time PCR and Western blotting.RESULTS: The levels of B7-H1,p-p38,p-ERK and p-JNK were up-regulated with LPS stimulation.The promoted p-p38,p-ERK and p-JNK levels induced by LPS were inhibited by the corresponding MAPKs inhibitors.Furthermore,the inhibitors of p38 and ERK attenuated LPS-induced B7-H1 expression.However,JNK inhibitor had very little effect on LPS-induced B7-H1 expression.CONCLUSION: LPS induces B7-H1 expression in pancreatic carcinoma cell line Panc-1.ERK and p38 are involved in this regulation as the inhibitors of ERK and p38 attenuate LPS-induced B7-H1 expression.
【Fund】: 浙江省重大科技专项重点社会发展项目(No.2011C13036-1)
【CateGory Index】: R735.9
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