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细胞因子通过JNK信号通路对内皮细胞蛋白C受体的调节 被引量:2

Regulation the expression of cytokineson on the endothelial protein C receptor through JNK signaling pathway
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摘要 目的观察细胞因子是否可通过JNK信号通路调节内皮细胞蛋白C受体的表达。方法分别检测用胎牛血清、TNF-α、IL-1β、IFN-γ及IL-4培养的人脐静脉内皮细胞EPCRmRNA、蛋白及磷酸化P38蛋白的表达。结果与对照组比较,TNF-α组、IL-1β组的EPCRmRNA含量均显著下降(均P<0.01),且IL-1β组EPCR蛋白含量明显下降(P<0.01);TNF-α组EPCR蛋白含量亦明显下降(P<0.05);TNF-α组、IL-1β组磷酸化JNK蛋白含量均显著增高(均P<0.01)。结论细胞因子TNF-α、IL-1β可从基因、蛋白水平减少人脐静脉内皮细胞上EPCR的表达,其调节机制可能是通过增加JNKMAPK实现的。 Objective To observe whether cytokineson can regulate the expression of endothelial protein C receptor through JNK signaling pathway. Methods The EPCR mRNA, protein and phosphor protein of JNK in HUVECs cultured with fetal blood serum. The TNF - α, IL - 1 β, IFN -γ and IL- 4 were detected, respectively. Results The expression of EPCR mRNA were significantly lower in TNF - α group, IL - 1 β group than that in normal control group (all P 〈 0. 01 ). The expression of EPCR protein was significantly lower in IL - 1 β group than that in normal control group (P 〈 0.01 ). The expression of EPCR protein was significantly lower in TNF - α group than that in normal control group (P 〈 0. 05 ). The expression of phosphor - JNK protein were significantly higher in TNF - αgroup, IL - 1β group than that in normal control group ( all P〈 0.01). Conclusion TNF-α,IL-1β could decrease EPCR mRNA and protein expression of HUVECs. Which maybe through increasing the expression of phosphor -JNK MAPK to come true.
出处 《中国临床药理学杂志》 CAS CSCD 北大核心 2010年第7期518-521,共4页 The Chinese Journal of Clinical Pharmacology
关键词 肿瘤坏死因子-Α 白介素-1Β 人脐静脉内皮细胞 内皮细胞蛋白C受体 tumor necrosis factor - α interleukin - 1 β human umbilical vein endothelial cells endothelial protein C receptor
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