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Articles in PresS, published online ahead of print July 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01001.2001
Submitted on November 15, 2001
Accepted on July 23, 2002
1 Department of Surgery, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA
* To whom correspondence should be addressed. E-mail: gbulkley{at}jhmi.edu.
Endothelial cell ICAM-1 upregulation in response to TNF-
is mediated in part by reactive oxygen species (ROS) generated by the endothelial membrane-associated NADPH oxidase, and occurs maximally after four hours, as the synthesis of new protein is required. However, thrombin-stimulated P-selectin upregulation is bimodal, the first peak occurring within minutes. We hypothesize that this early peak, which results from the release of preformed P-selectin from within Weibel-Palade bodies, is mediated in part by ROS generated from the endothelial membrane-associated xanthine oxidase. This rapid expression of P-selectin on the surface of endothelial cells was accompanied by qualitatively parallel increases in ROS generation. Both P-selectin expression and ROS generation were inhibited, dose-dependently, by the exogenous administration of disparate cell-permeable antioxidants, and also by the inhibition of either of the known membrane-associated ROS generating enzymes, NADPH oxidase or xanthine oxidase. This rapid, post-translational cell signaling response, mediated by ROS generated not only by the classical NADPH oxidase but also by xanthine oxidase, may well represent an important physiologic trigger of the microvascular inflammatory response.
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