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Am J Physiol Gastrointest Liver Physiol 278: G878-G885, 2000;
0193-1857/00 $5.00
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Vol. 278, Issue 6, G878-G885, June 2000

Regulation of E-selectin expression in postischemic intestinal microvasculature

Janice Russell1, Charles J. Epstein2, Matthew B. Grisham1, J. Steven Alexander1, Kwoh-Yih Yeh1, and D. Neil Granger1

1 Departments of Molecular and Cellular Physiology and Medicine, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932; and 2 Department of Pediatrics, University of California, San Francisco, California 94143-0748

Monolayers of cultured endothelial cells exposed to hypoxia-reoxygenation exhibit a transcription-dependent increase in E-selectin expression and E-selectin-dependent neutrophil-endothelial cell adhesion. The overall objectives of this study were 1) to determine whether ischemia-reperfusion (I/R) promotes upregulation of E-selectin in vivo; 2) if so, to define the mediators of this response; and 3) to assess the contribution of E-selectin to I/R-induced neutrophil recruitment. The dual-radiolabeled monoclonal antibody (MAb) technique was used to measure E-selectin expression in the intestinal vasculature. Ischemia was induced by complete occlusion (30-60 min) of the superior mesenteric artery followed by 3-24 h of reperfusion. Increasing durations of ischemia elicited progressively increasing (2- to 5-fold) levels of E-selectin expression, with the peak response noted after 45 min of ischemia and 5 h of reperfusion. Subsequent experiments revealed that I/R-induced increase in E-selectin expression (at 5 h) is significantly blunted in transgenic mice that overexpress Cu,Zn-superoxide dismutase or by treatment of wild-type mice with either a blocking antibody against tumor necrosis factor (TNF)-alpha or an inhibitor of nuclear factor-kappa B (NF-kappa B) activation (PS341). Administration of an E-selectin-specific MAb dramatically reduced I/R-induced recruitment of neutrophils in the intestine. These findings suggest that superoxide and TNF-alpha mediate gut I/R-induced E-selectin expression via an NF-kappa B-dependent mechanism; this upregulation of E-selectin contributes significantly to I/R-induced neutrophil recruitment.

superoxide dismutase; tumor necrosis factor; neutrophils; nuclear factor-kappaB; interferon-gamma


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