Contribution of cyclooxygenase-1 to thromboxane formation, platelet-vessel wall interactions and atherosclerosis in the ApoE null mouse.

摘要: Abstract Objective Prostaglandin and thromboxane (TXA 2 ) generation is increased in atherosclerosis. Studies with selective inhibitors attribute the enhanced prostacyclin (PGI to both cyclooxygenase-1 (COX-1) COX-2 whereas TXA reflects platelet COX-1 expression. However, formation remains elevated patients cardiovascular disease on doses of aspirin that fully suppress COX-1, suggesting other tissue sources for formation. Disruption receptor gene suppresses development Notwithstanding this, role atherosclerosis unclear, as it widely distributed contributes a number products, including those potentially contribute resolution inflammation. Methods results We examined prostaglandin generation, platelet–vessel wall interactions apoE −/− murine model by disrupting gene. ApoE /COX-1 +/+ , +/− were administered 1% cholesterol diet 8 weeks. Stable urinary metabolites PGI which markedly reduced disruption COX-1. Deletion one or copies suppressed lesion Assessment intravital microscopy showed significant decrease firm adhesion platelets apoE/COX-1 double knockout (DKO). Conclusion atherosclerosis, disease. Non-platelet are inaccessible standard may