What is it about?
The therapeutic effects of aspirin are due to inhibition of prostaglandin biosynthesis by the cyclooxygenase enzymes (COX-1 and COX-2). Prostaglandins are important mediators of inflammation. Here we describe that aspirin-treated COX-2 retains an ability to form prostaglandins albeit one of the stereocenters is mostly inverted from the 15S to the 15R configuration. 15R-Prostaglandins are formed by human leukocytes in response to treatment with aspirin. They show favorable biologic effects by inhibiting platelet aggregation. Thus, aspirin not only inhibits formation of pro-aggregatory thromboxane by inhibition of platelet COX-1 but also triggers formation of anti-aggregatory 15R-prostaglandins by acetylation of COX-2 in leukocytes.
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Why is it important?
The novel activity of COX-2 may represent a previously unrecognized cardioprotective mechanism of aspirin therapy.
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This page is a summary of: Residual cyclooxygenase activity of aspirin-acetylated COX-2 forms 15R-prostaglandins that inhibit platelet aggregation, The FASEB Journal, January 2019, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201801018r.
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