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Thromboxane A2 is a mediator of cyclooxygenase-2-dependent endothelial migration and angiogenesis
T O Daniel1, H Liu, J D Morrow
1Department of Medicine, The Vanderbilt Center for Vascular Biology, Vanderbilt University, Nashville, Tennessee 37232, USA. tom.daniel@mcmail.vanderbilt.edu
Abstract:
Cyclooxygenase-2 (COX-2) inhibitors reduce angiogenic responses to a variety of stimuli, suggesting that products of COX-2 may mediate critical steps. Here, we show that thromboxane A2 (TXA2) is one of several eicosanoid products generated by activated human microvascular endothelial cells. Selective COX-2 antagonists inhibit TXA2 production, endothelial migration, and fibroblast growth factor-induced corneal angiogenesis. Endothelial migration and corneal angiogenesis are similarly inhibited by a TXA2 receptor antagonist, SQ29548. A TXA2 agonist, U46619, reconstitutes both migration and angiogenesis responses under COX-2-inhibited conditions. These findings identify TXA2 as a COX-2 product that functions as a critical intermediary of angiogenesis.