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[Cancer Research 59, 4574-4577, September 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 4574-4577, September 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Thromboxane A2 Is a Mediator of Cyclooxygenase-2-dependent Endothelial Migration and Angiogenesis1

Thomas O. Daniel2, Hua Liu, Jason D. Morrow, Brenda C. Crews and Lawrence J. Marnett

Departments of Medicine, Cell Biology, Biochemistry, and Pharmacology, Divisions of Nephrology and Hypertension and Clinical Pharmacology, The Vanderbilt Center for Vascular Biology, Vanderbilt Cancer Center, Vanderbilt University, Nashville, Tennessee 3723

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.




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