15-Hydroxyprostaglandin dehydrogenase. A review

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      Notably, Ptgfr has been reported in tibial nerve in humans,27 and in endometrium31 while Ptgir has been observed mainly in blood vessels.19,27 One of the major pathways by which PGE2 is degraded is via the oxidation of the 15(S)-hydroxyl group of prostaglandin E2 by 15-hydroxyprostaglandin dehydrogenase, reducing this mediator to less reactive metabolites.29 This enzyme has been reported in human skin27 and we found here that this transcript was enriched in rat hind paw (sFPKM = 19) relative to other pain circuit tissues (sFPKM <1.3), pointing towards a basal reservoir of enzyme capable of degrading prostanoids, which are generally produced on-demand.

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      Prostanoids, (except 15-dPGJ2) have in common a hydroxyl group at carbon 15 that is targeted by the endothelial 15-prostaglandin dehydrogenase (15-PGDH), an NAD-dependent dehydrogenase of this secondary alcohol. 15-PGDH is known to be especially efficient in pulmonary circulation, allowing the formation of 15-oxo-PGs that lose a great part of their biological activities, meaning that most circulating prostanoids will become inactive after a few pulmonary passages [40]. The 15-oxo-PGs derived from this process are further degraded to the 13,14-dehydro-15-oxo-PGs by NADPH reduction [41].

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