Prostaglandin Receptor

Prostaglandin Receptor

Prostaglandin receptor, a sub-family of cell surface seven-transmembrane receptors, are the G-protein-coupled receptors. There are currently ten known prostaglandin receptors on various cell types.

An overview of Prostaglandin receptor

Prostanoids consist of prostaglandins (PGs) and thromboxanes (TX) and are products of cyclooxygenase derived from arachidonic acid, which is the most abundant precursor fatty acid in mammals. PGs are a group of lipid mediators formed in response to various stimuli. They include PGD2, PGE2, PGF2α and PGI2. They are released outside of the cells immediately after synthesis, and exert their actions by binding to a G-protein coupled rhodopsin-type receptor on the surface of target cells. Prostaglandin receptors, a sub-family of cell surface seven-transmembrane receptors, are the G-protein coupled receptors. There are seven types of the prostanoid receptors conserved in mammals from mouse to human. They are the PGD receptor (DP), four subtypes of the PGE receptor (EP1, EP2, EP3, and EP4), the PGF receptor (FP) and PGI receptor (IP). The roles of PGs and their receptor signaling in various physiological and pathophysiological conditions have been examined by comparing the effects of aspirin-like drugs with those of each prostanoid added exogenously.

Antagonist of Prostaglandin receptor

Characterization of these receptors at the molecular level has resulted in renewed interest in this field, but few selective agonists and antagonists of human prostanoid receptors are available. A lot of N-(palkoxy) benzoyl-2-methylindole-4-acetic acids were reported and identified as a new class of selective PGs receptor antagonists. Most of them showed strong PGD2 receptor antagonism in binding studies and the cAMP formation assay.

Prostaglandin receptor and diseases

Among the various PGs, PGI2 and PGE2 have been implicated as the PGs most responsible for inflammation because of their abundance in inflammatory exudates and tissues and their ability to mimic inflammatory responses by their administration in vivo. It has been proposed that excess production of PGD2 also causes the inflammation commonly observed in allergic diseases such as allergic rhinitis, asthma, and atopic dermatitis. Besides, some studies have revealed the critical PG receptor signaling pathways for promoting acute inflammation and the context-dependent effects of this signaling, which could be determined by the types and the phases of inflammation.


Toshiyuki Matsuoka (2007). Prostaglandin Receptor Signaling in Disease, 182, 7, 1329–1347.Kazuhiko Torisu (2004). Development of prostaglandin D2 receptor antagonist: discovery of highly potent antagonists, 12,4765-4700.

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