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首页> 外文期刊>Biochimica et biophysica acta. Molecular cell research >Tryptase activates PKB in inflammatory reaction in ECV304 cells
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Tryptase activates PKB in inflammatory reaction in ECV304 cells

机译:类胰蛋白酶激活ECV304细胞炎症反应中的PKB

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Tryptase is involved in proteinase-activated receptor-2 (PAR-2) mediated up-regulation of IL-8 expression. The present report showed the effects of tryptase on gene expression and activation, including up-regulation IL-8 expression. The expression of rnRNA for NF-kappa B first increased at I h after tryptase-treatment (1 ng/ml) and reached the plateau after 4 h. The NF-kappa B mRNA increased by 3-fold (n=3, P < 0.05), AP-1 by 2-fold (n=3, P < 0.05), and PKB by 10-fold (n=3, P < 0.05). However, tryptase-treatment did not affect the expression of JNK and p38 MAPK when compared with control cells at mRNA level. Furthermore, in addition to increasing phosphorylation of p38 MAPK, tryptase-treatment also increased phosphorylation of PKB by 2-fold at 15 min following the treatment. The up-regulation and phosphorylation of PKB by tryptase could be abolished by either phosphoinositol-3-kinase (PI3K) inhibitor (LY294002) at 10 mu M or antisense PKB cDNA transfection. The up-regulation of NF-kappa B expression could be inhibited by LY294002 and antisense PKB cDNA. These results indicate that tryptase can activate PI3K-PKB pathway and enhance IL-8 expression. (c) 2006 Elsevier B.V. All rights reserved.
机译:类胰蛋白酶参与蛋白酶激活受体2(PAR-2)介导的IL-8表达的上调。本报告显示了类胰蛋白酶对基因表达和激活的影响,包括上调IL-8表达。胰蛋白酶处理(1 ng / ml)后1小时,NF-κB的rnRNA表达首先增加,并在4小时后达到稳定水平。 NF-κBmRNA增加3倍(n = 3,P <0.05),AP-1增加2倍(n = 3,P <0.05),PKB增加10倍(n = 3,P <0.05)。但是,与mRNA水平的对照细胞相比,类胰蛋白酶处理不影响JNK和p38 MAPK的表达。此外,除了增加p38 MAPK的磷酸化外,在处理后15分钟,类胰蛋白酶处理还使PKB的磷酸化增加了2倍。胰蛋白酶3激酶(PI3K)抑制剂(LY294002)在10μM或反义的PKB cDNA转染可消除类胰蛋白酶对PKB的上调和磷酸化作用。 LY294002和反义PKB cDNA可抑制NF-κB表达的上调。这些结果表明类胰蛋白酶可以激活PI3K-PKB途径并增强IL-8表达。 (c)2006 Elsevier B.V.保留所有权利。

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