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J Appl Physiol 90: 2279-2288, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 6, 2279-2288, June 2001

Role of thromboxane in retinal microvascular degeneration in oxygen-induced retinopathy

Martin H. Beauchamp1, Ana Katherine Martinez-Bermudez1,2, Fernand Gobeil Jr.1, Anne Marilise Marrache1,2, Xin Hou1, Giovanna Speranza1,2, Daniel Abran1, Christiane Quiniou1, Pierre Lachapelle3, Jackson Roberts II4, Guillermina Almazan2, Daya R. Varma2, and Sylvain Chemtob1,2

1 Departments of Pediatrics, Ophthalmology and Pharmacology, Research Center, Hôpital Sainte-Justine, Montreal, Quebec H3T 1C5; Departments of 2 Pharmacology and Therapeutics and 3 Ophthalmology, McGill University, Montreal, Quebec, Canada H3G 1Y6; and 4 Departments of Pharmacology and Medicine, Vanderbilt University, Nashville, Tennessee 37232-6602

Microvascular degeneration is an important event in oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity. Because oxidant stress abundantly generates thromboxane A2 (TxA2), we tested whether TxA2 plays a role in retinal vasoobliteration of OIR and contributes to such vascular degeneration by direct endothelial cytotoxicity. Hyperoxia-induced retinal vasoobliteration in rat pups (80% O2 exposure from postnatal days 5-14) was associated with increased TxB2 generation and was significantly prevented by TxA2 synthase inhibitor CGS-12970 (10 mg · kg-1 · day-1) or TxA2-receptor antagonist CGS-22652 (10 mg · kg-1 · day-1). TxA2 mimetics U-46619 (EC50 50 nM) and I-BOP (EC50 5 nM) caused a time- and concentration-dependent cell death of neuroretinovascular endothelial cells from rats as well as newborn pigs but not of smooth muscle and astroglial cells; other prostanoids did not cause cell death. The peroxidation product 8-iso-PGF2, which is generated in OIR, stimulated TxA2 formation by endothelial cells and triggered cell death; these effects were markedly diminished by CGS-12970. TxA2-dependent neuroretinovascular endothelial cell death was mostly by necrosis and to a lesser extent by apoptosis. The data identify an important role for TxA2 in vasoobliteration of OIR and unveil a so far unknown function for TxA2 in directly triggering neuroretinal microvascular endothelial cell death. These effects of TxA2 might participate in other ischemic neurovascular injuries.

endothelium; retina; necrosis; apoptosis; peroxidation


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