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Prostaglandin Receptor
When tissues are exposed to diverse physiological and pathological stimuli, arachidonic acid (AA) is liberated from membrane phospholipids and is converted to prostanoids, including the prostaglandins (PGs) and the thromboxanes (TXs), by the action of cyclooxygenase (COX). There are eight types and subtypes of receptors for prostanoid that are conserved in mammals from mouse to human: the PGD receptor (DP), four subtypes of the PGE receptor (EP1, EP2, EP3, and EP4), the PGF receptor (FP), the PGI receptor (IP), and the TXA receptor (TP). 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.
Among the various PG species, 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. PGE2, PGE1, and PGI2 exert stronger effects than the other types of PGs, indicating the involvement of these two signaling pathways via EP or IP receptors in inducing inflammatory pain. PGE2 released into the brain may act on the neurons expressing EP receptors in the anteromedial preoptic area of the hypothalamus (POA), where expression of EP1, EP3, and EP4 receptors are demonstrated in rat. In view of molecular mechanisms of PGD2-DP signaling in allergic asthma, it is reported that PGD2-DP signaling is mediated via p38 MAPK, p44/42 MAPK, and PKC in a cell type-specific manner leading to NF-kB activation stimulating COX-2 gene expression. Thus, selective manipulation of the prostanoid receptors may be beneficial in treatment of the pathological conditions.
Among the various PG species, 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. PGE2, PGE1, and PGI2 exert stronger effects than the other types of PGs, indicating the involvement of these two signaling pathways via EP or IP receptors in inducing inflammatory pain. PGE2 released into the brain may act on the neurons expressing EP receptors in the anteromedial preoptic area of the hypothalamus (POA), where expression of EP1, EP3, and EP4 receptors are demonstrated in rat. In view of molecular mechanisms of PGD2-DP signaling in allergic asthma, it is reported that PGD2-DP signaling is mediated via p38 MAPK, p44/42 MAPK, and PKC in a cell type-specific manner leading to NF-kB activation stimulating COX-2 gene expression. Thus, selective manipulation of the prostanoid receptors may be beneficial in treatment of the pathological conditions.
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