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Thromboxane (Tx) [A.sub.2] is a vasoconstrictor and platelet agonist. Aspirin affords cardioprotection through inhibition of Tx[A.sub.2] formation by platelet cyclooxygenase (COX-l). Prostacydin (PG[I.sub.2]) is a vasodilator that inhibits platelet function. Here we show that injury-induced vascular proliferation and platelet activation are enhanced in mice that are genetically deficient in the PG[I.sub.2] receptor (IP) but are depressed in mice genetically deficient in the Tx[A.sub.2] receptor (TP) or treated with a TP antagonist. The augmented response to vascular injury was abolished in mice deficient in both receptors. Thus, PG[I.sub.2] modulates platelet-vascular interactions in vivo and specifically limits the response to Tx[A.sub.2]. This interplay may help explain the adverse cardiovascular effects associated with selective COX-2 inhibitors, which, unlike aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), inhibit PG[I.sub.2] but not Tx[A.sub.2]., Prostacyclin (PG[I.sub.2]) is the major product of cyclooxygenase (COX) catalyzed metabolism of arachidonic acid in macrovascular endothelium (1, 2). It is a potent inhibitor of platelet activation by all recognized [...]

The article discusses the use of dimethyl Prostaglandin E2 (PGE2) as a supplement to hematopoietic stem cell transplantation to promote tissue regeneration. Topics include the suppression of prostaglandin (PG) formation by nonsteroidal anti-inflammatory drugs (NSAIDs), risks associated with the use of prostaglandin inhibitors to treat inflammatory disease, and increased hematopoiesis, liver regeneration, and resistance to colitis in mice from elevated PGE2 and reduced 15-PGHD by Zhang et al.

The article announces that pharmacologists Garret FitzGerald of the University of Pennsylvania and Carlo Patrono of the Catholic University in Rome, Italy won the 2013 Grand Prix Scientifique from the Institut de France for their work in cardiovascular health.

Thromboxane (Tx) A² is a vasoconstrictor and platelet agonist. Aspirin affords cardioprotection through inhibition of TxA² formation by platelet cyclooxy-genase (COX-1). Prostacyclin (PGI[sub 2]) is a vasodilator that inhibits platelet function. Here we show that injury-induced vascular proliferation and platelet activation are enhanced in mice that are genetically deficient in the PGI[sub 2] receptor (IP) but are depressed in mice genetically deficient in the TxA[sub 2] receptor (TP) or treated with a TP antagonist. The augmented response to vascular injury was abolished in mice deficient in both receptors. Thus, PGI[sub 2] modulates platelet-vascular interactions in vivo and specifically limits the response to TxA[sub 2]. This interplay may help explain the adverse cardiovascular effects associated with selective COX-2 inhibitors, which, unlike aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), inhibit PGI[sub 2] but not TxA[sub 2]. [ABSTRACT FROM AUTHOR]