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首页> 外文期刊>Cytokine >Transcriptional regulation of the human interleukin 1beta gene by fibronectin: role of protein kinase C and activator protein 1 (AP-1).
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Transcriptional regulation of the human interleukin 1beta gene by fibronectin: role of protein kinase C and activator protein 1 (AP-1).

机译：纤连蛋白对人类白介素1beta基因的转录调控：蛋白激酶C和激活蛋白1（AP-1）的作用。

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摘要

Interleukin 1beta (IL-1beta) is a multifunctional polypeptide considered a key cytokine during inflammation. Fibronectin (FN), a matrix glycoprotein highly expressed in injured tissues, can induce expression of IL-1beta in human blood monocytic cells. Herein, we explore the intracellular signals and transcriptional mechanisms responsible for IL-1beta induction by FN using human promonocytic U937 cells transfected with the human IL-1beta promoter connected to a reporter gene. Exposure of transfected U937s to FN resulted in increased expression of the full-length IL-1beta promoter. This effect, mediated via the alpha5beta1 integrin, was associated with activation of mitogen-activated protein kinases (MAPKs) and was abolished by pre-treatment of cells with Calphostin C, a specific inhibitor of protein kinase C (PKC) activation. Deletion analysis and co-transfection studies using consensus activator protein 1 (AP-1) oligonucleotides suggested that an AP-1 site present in the 5' end of the IL-1beta promoter was involved in the FN-induced response. Finally, electrophoretic mobility shift assays showed that FN induced binding of AP-1, but not NF-kappaB. Together, these experiments demonstrate that FN binding to the alpha5beta1 integrin activates MAPK-dependent signal pathways, and results in the transcription of the IL-1beta promoter in U937 cells by activating PKC and inducing AP-1. Copyright 2000 Academic Press.
机译：白介素1beta（IL-1beta）是一种多功能多肽，被认为是炎症过程中的关键细胞因子。纤连蛋白（FN）是一种在受损组织中高表达的基质糖蛋白，可诱导人血单核细胞中IL-1β的表达。在这里，我们探索细胞内信号和转录机制负责通过使用连接到报告基因的人IL-1β启动子转染的人原单核细胞U937细胞通过FN诱导IL-1beta。转染的U937s暴露于FN导致全长IL-1beta启动子的表达增加。这种作用是通过alpha5beta1整合素介导的，与丝裂原激活的蛋白激酶（MAPK）的激活有关，并通过用钙磷蛋白C（一种蛋白激酶C（PKC）激活的特异性抑制剂）预处理细胞而被取消。使用共有激活蛋白1（AP-1）寡核苷酸进行的缺失分析和共转染研究表明，IL-1beta启动子5'端存在的AP-1位点参与了FN诱导的应答。最后，电泳迁移率变动分析表明FN诱导了AP-1的结合，但不诱导NF-κB的结合。总之，这些实验表明，FN与alpha5beta1整联蛋白的结合可激活MAPK依赖性信号通路，并通过激活PKC和诱导AP-1导致U937细胞中IL-1beta启动子的转录。版权所有2000学术出版社。

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