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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Selective activation of endothelial cells by the antioxidant pyrrolidine dithiocarbamate: involvement of C-jun N-terminal kinase and AP-1 activation.
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Selective activation of endothelial cells by the antioxidant pyrrolidine dithiocarbamate: involvement of C-jun N-terminal kinase and AP-1 activation.

机译：抗氧化剂吡咯烷二硫代氨基甲酸酯对内皮细胞的选择性激活：涉及C-jun N端激酶和AP-1激活。

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摘要

The antioxidant agent pyrrolidine dithiocarbamate (PDTC) has been shown to protect endothelial cells (EC) from pro-inflammatory-induced and pro-oxidant-induced NF-kappaB activation. It also perturbs EC by altering activator protein-1 (AP-1) status and inducing ICAM-1. Experiments were performed to investigate the upstream mechanism by which PDTC produces these effects. We have demonstrated that PDTC not only induced AP-1 binding and ICAM-1 expression by itself, but it also augmented AP-1 activation and ICAM-1 induction in low-dose IL-1alpha treated cells. To dissect the mechanism of these effects, we measured c-Jun and c-Fos expression, and the activity of c-Jun NH2-terminal kinase (JNK) and extracellular signal regulated kinase (ERK) in human umbilical vein endothelial cells (HUVEC). We detected an increase in JNK activity in PDTC-treated HUVEC. Following cotransfection with JNK[K-M], a kinase-deficient JNK1, the PDTC-increased AP-1-driven-luciferase activity was attenuated. Utilizing a specific trans-reporting system we confirmed c-Jun activation by upstream signaling mechanisms. The results show that c-Jun activity was increased 9-fold after PDTC treatment. In addition, PDTC promoted more transient activation in ERK-c-fos. In contrast, PDTC produced sustained JNK-c-Jun activation, which translated into long-lasting ICAM-1 production. These results suggest that an antioxidant may contribute to chronic vascular endothelial activation.
机译：抗氧化剂吡咯烷二硫代氨基甲酸酯（PDTC）已显示可保护内皮细胞（EC）免受促炎性和促氧化剂诱导的NF-κB活化。它还通过改变激活蛋白-1（AP-1）状态和诱导ICAM-1干扰EC。进行实验以研究PDTC产生这些作用的上游机制。我们已经证明PDTC本身不仅诱导AP-1结合和ICAM-1表达，而且在低剂量IL-1alpha处理的细胞中还增强了AP-1活化和ICAM-1诱导。为了剖析这些效应的机制，我们测量了人脐静脉内皮细胞（HUVEC）中c-Jun和c-Fos的表达以及c-Jun NH2末端激酶（JNK）和细胞外信号调节激酶（ERK）的活性。我们检测到PDTC处理的HUVEC中JNK活性增加。与激酶缺陷的JNK1 JNK [K-M]共转染后，PDTC增加的AP-1驱动的荧光素酶活性减弱。利用特定的报告系统，我们通过上游信号传导机制证实了c-Jun的激活。结果表明，PDTC处理后c-Jun活性增加了9倍。另外，PDTC促进了ERK-c-fos中更多的瞬时激活。相反，PDTC产生了持续的JNK-c-Jun激活，转化为持久的ICAM-1产生。这些结果表明抗氧化剂可能有助于慢性血管内皮的活化。

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