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Am J Physiol Cell Physiol (January 29, 2003). doi:10.1152/ajpcell.00243.2002
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Submitted on May 28, 2002
Accepted on January 26, 2003

The Effect of Interleukin-1 beta and Tumor Necrosis Factor alpha on Gene Expression in Human Endothelial Cells

Baiteng Zhao1, Salomon A Stavchansky2, Robert A Bowden3, and Phillip D Bowman3*

1 College of Pharmacy, Pharmaceutics Division, University of Texas at Austin, Austin, Texas, USA; U.S. Army Institute of Surgical Research and Clinical Investigation, Brook Army Medical Center, San Antonio, Texas, USA
2 College of Pharmacy, Pharmaceutics Division, University of Texas at Austin, Austin, Texas, USA
3 U.S. Army Institute of Surgical Research and Clinical Investigation, Brook Army Medical Center, San Antonio, Texas, USA

* To whom correspondence should be addressed. E-mail: phillip.bowman{at}amedd.army.mil.

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




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