Prostaglandin receptors or prostanoid receptors represent a sub-class of cell surface membrane receptors that are regarded as the primary receptors for one or more of the classical, naturally occurring prostanoids viz., prostaglandin D2, (i.e. PGD2), PGE2, PGF2alpha, prostacyclin (PGI2), thromboxane A2 (TXA2), and PGH2.[1] They are named based on the prostanoid to which they preferentially bind and respond, e.g. the receptor responsive to PGI2 at lower concentrations than any other prostanoid is named the Prostacyclin receptor (IP). One exception to this rule is the receptor for thromboxane A2 (TP) which binds and responds to PGH2 and TXA2 equally well.
All of the prostanoid receptors are G protein-coupled receptors belonging to the Subfamily A14 of the rhodopsin-like receptor family except for the Prostaglandin DP2 receptor which is more closely related in amino acid sequence and functionality to chemotactic factor receptors such as the receptors for C5a and leukotriene B4.[2]
Prostanoid receptors bind and respond principally to metabolites of the straight chain polyunsaturated fatty acid (PUFA), arachidonic acid. These metabolites contain two double bonds and are named series 2 prostanoids, i.e. PGD2, PGE2, PGF2α, PGI2, TXA2 and PGH2. However, the same enzymes that metabolize arachidonic acid to series 2 prostanoids similarly metabolize two other straight chain PUFAs: they metabolize gamma-Linolenic acid, which has one less double bond than arachidonic acid, to series 1 prostanoids (PGD1, PGE1, etc.), which have one less double bond than the series 2 prostanoids, and they metabolize eicosapentaenoic acid, which has one more double bond than arachidonic acid, to series 3 prostanoids (PGD3, PGE3, etc.), which have one more double bond than the series 2 prostanoids. In general, receptors for the series 2 prostanoids also bind with and respond to the series 1 and 3 prostanoids. Typically, prostanoid receptors show somewhat less affinity and responsiveness to the 1 and 3 series prostanoids.[3]
There is indirect evidence for a second PGI2 receptor in BEAS-2B human airway epithelial cells but this finding has not been collaborated and the putative receptor has not been otherwise defined.[15]
^Wilson SM, Sheddan NA, Newton R, Giembycz MA (2011). "Evidence for a second receptor for prostacyclin on human airway epithelial cells that mediates inhibition of CXCL9 and CXCL10 release". Molecular Pharmacology. 79 (3): 586–95. doi:10.1124/mol.110.069674. PMID21173040. S2CID11882621.