Thromboxane A2 is a mediator of cyclooxygenase-2-dependent endothelial migration and angiogenesis
| Autor: | T O, Daniel, H, Liu, J D, Morrow, B C, Crews, L J, Marnett |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Neovascularization
Physiologic Dinoprost Dinoprostone Renal Circulation Cornea Mice Thromboxane A2 Cell Movement Animals Humans Cyclooxygenase Inhibitors Cells Cultured Cyclooxygenase 2 Inhibitors Neovascularization Pathologic Microcirculation Membrane Proteins Bridged Bicyclo Compounds Heterocyclic Fibroblast Growth Factors Isoenzymes Mice Inbred C57BL Hydrazines Cyclooxygenase 2 Prostaglandin-Endoperoxide Synthases 15-Hydroxy-11 alpha 9 alpha-(epoxymethano)prosta-5 13-dienoic Acid Fatty Acids Unsaturated Tetradecanoylphorbol Acetate Fibroblast Growth Factor 2 Endothelium Vascular |
| Zdroj: | Cancer research. 59(18) |
| ISSN: | 0008-5472 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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