Abstract
The prostanoids are a family of lipid mediators generated by the action of cyclooxygenase on a 20-carbon unsaturated fatty acid, arachidonic acid. Prostanoids are generated widely in response to diverse stimuli and, acting in a paracrine or autocrine manner, play important roles in normal physiology and disease. This review summarizes the current knowledge on prostanoid generation and the roles of individual mediators, their biosynthetic pathways, and their receptors in health and disease.
Highlights
The prostanoids are a family of lipid mediators generated by the action of cyclooxygenase on a 20-carbon unsaturated fatty acid, arachidonic acid
COX-2 prefers prostaglandin I synthase (PGIS) and the microsomal (m) prostaglandin E synthase (PGES) isozymes, both of which are induced by cytokines and tumor promoters
We recently found that selective deletion of cardiomyocyte COX-2 resulted in heart failure and cardiac fibrosis in mice, demonstrating a direct role of COX-2-derived prostanoids in cardiac function
Summary
Prostanoids are formed by the action of prostaglandin G/H synthase, or cyclooxygenase (COX), on AA. Prostanoids activate membrane receptors at, or close to, the site of their formation. Specific G-protein-coupled receptors have been cloned for all the prostanoids [5]. EP2, EP4, IP, and DP1 receptors activate adenylyl cyclase via Gs, increasing intracellular cAMP. TP couples to multiple G proteins, including G12/13 and G16, to stimulate small G protein signaling pathways and may activate or inhibit adenylyl cyclase. EP3 isoforms can couple via Gi or G12 to elevation of intracellular Ca21, inhibition of cAMP generation, and activation of the small G protein Rho. The DP2 ( known as the chemoattractant receptor homologous molecule expressed on Th2 cells) couples to a Gi-type G protein to inhibit cAMP synthesis and elevate intracellular Ca21
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