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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Gene expression of endothelial cells due to interleukin-1 beta stimulation and neutrophil transmigration.
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Gene expression of endothelial cells due to interleukin-1 beta stimulation and neutrophil transmigration.

机译：由于白介素-1β刺激和嗜中性粒细胞迁移，内皮细胞的基因表达。

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During the inflammatory response, endothelial cell (EC) functions and mechanics change dramatically. To understand these responses, the authors analyzed changes in EC gene expression in an in vitro model of inflammation using cDNA microarrays. After interleukin-1 beta (IL1beta) stimulation, over 2500 genes were differentially expressed, of which approximately 2000 had not been previously identified by microarray studies of IL1beta stimulation in human umbilical vein endothelial cells (HUVECs). Functional grouping of these genes according to gene ontologies revealed genes associated with apoptosis, cell cycle, nuclear factor (NF)-kappa B cascade, chemotaxis, and immune response. Interestingly, claudin-1, known to exist in endothelial cell-cell junctions was up-regulated, but claudin-5 and occludin, which also exist in EC junctions, were down-regulated. Pre-b-cell colony enhancing factor (PBEF), a cytokine which may play a role in regulating endothelial permeability, was also up-regulated following IL1beta stimulation. Neutrophil transmigration across IL1beta-stimulated ECs did not induce changes in EC gene expression as strongly as IL1beta stimulation alone. Nineteen genes after 1 h and 22 genes after 3 h of neutrophil application were differentially expressed. These results indicate that, in terms of transcriptional effects on ECs, neutrophil transmigration is a relatively small perturbation in comparison to the background of large scale changes induced in ECs by cytokine stimulation. Supplementary materials are available for this article. Go to the publisher's online edition of Endothelium for the following free supplementary resources: supplementary figures and tables.
机译：在炎症反应期间，内皮细胞（EC）的功能和机制会发生巨大变化。为了理解这些反应，作者使用cDNA微阵列分析了体外炎症模型中EC基因表达的变化。在白介素-1β（IL1beta）刺激后，差异表达了2500多个基因，其中以前在人脐静脉内皮细胞（HUVECs）中通过IL1beta刺激的微阵列研究尚未鉴定出约2000个基因。这些基因根据基因本体的功能分组揭示了与凋亡，细胞周期，核因子（NF）-κB级联，趋化性和免疫反应相关的基因。有趣的是，已知存在于内皮细胞-细胞连接中的claudin-1被上调，但是也存在于EC连接中的claudin-5和occludin被下调。在IL1beta刺激后，前b细胞集落增强因子（PBEF），一种可能在调节内皮通透性中起作用的细胞因子，也被上调。嗜中性粒细胞跨IL1beta刺激的EC的迁移不会像单独IL1beta刺激那样强烈地诱导EC基因表达的变化。嗜中性粒细胞应用1小时后有19个基因和3小时后有22个基因差异表达。这些结果表明，就对ECs的转录作用而言，与细胞因子刺激在ECs中引起的大规模变化的背景相比，嗜中性白细胞的迁移是相对较小的扰动。补充材料可用于本文。有关以下免费的补充资源，请访问出版商的内皮细胞在线版：补充数字和表格。

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