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白细胞介素-1β和肿瘤坏死因子-α对人内皮细胞基因表达的影响。

Effect of interleukin-1beta and tumor necrosis factor-alpha on gene expression in human endothelial cells.

作者信息

Zhao Baiteng, Stavchansky Salomon A, Bowden Robert A, Bowman Phillip D

机构信息

Pharmaceutics Division, College of Pharmacy, University of Texas at Austin, Austin 78712, USA.

出版信息

Am J Physiol Cell Physiol. 2003 Jun;284(6):C1577-83. doi: 10.1152/ajpcell.00243.2002. Epub 2003 Jan 29.

Abstract

Interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are two major cytokines that rise to relatively high levels during systemic inflammation, and the endothelial cell (EC) response to these cytokines may explain some of the dysfunction that occurs. To better understand the cytokine-induced responses of EC at the gene expression level, human umbilical vein EC were exposed to IL-1beta or TNF-alpha for various times and subjected to cDNA microarray analyses to study alterations in their mRNA expression. Of approximately 4,000 genes on the microarray, expression levels of 33 and 58 genes appeared to be affected by treatment with IL-1beta and TNF-alpha, respectively; 25 of these genes responded to both treatments. These results suggest that the effects of IL-1beta and TNF-alpha on EC are redundant and that it may be necessary to suppress both cytokines simultaneously to ameliorate the systemic response.

摘要

白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)是两种主要的细胞因子,在全身炎症期间会升高到相对较高的水平,内皮细胞(EC)对这些细胞因子的反应可能解释了所发生的一些功能障碍。为了在基因表达水平上更好地理解细胞因子诱导的内皮细胞反应,将人脐静脉内皮细胞暴露于IL-1β或TNF-α不同时间,并进行cDNA微阵列分析以研究其mRNA表达的变化。在微阵列上约4000个基因中,分别有33个和58个基因的表达水平似乎受到IL-1β和TNF-α处理的影响;其中25个基因对两种处理均有反应。这些结果表明,IL-1β和TNF-α对内皮细胞的作用是冗余的,可能有必要同时抑制这两种细胞因子以改善全身反应。

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