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Prostaglandin F 2α  (PGF 2α ), represses ovarian steroidogenesis and initiates parturition in mammals but its impact on adrenal gland is unknown. Prostaglandins biosynthesis depends on the sequential action of upstream cyclooxygenases (COX) and terminal synthases but no PGF 2α  synthases (PGFS) were functionally identified in mammalian cells.  In vitro , the most efficient mammalian PGFS belong to aldo-keto reductase 1B (AKR1B) family. The adrenal gland is a major site of AKR1B expression in both human (AKR1B1) and mouse (AKR1B3, AKR1B7). Thus, we examined the PGF 2α  biosynthetic pathway and its functional impact on both cortical and medullary zones. Both compartments produced PGF 2α  but expressed different biosynthetic isozymes. In chromaffin cells, PGF 2α  secretion appeared constitutive and correlated to continuous expression of COX1 and AKR1B3. In steroidogenic cells, PGF 2α  secretion was stimulated by adrenocorticotropic hormone (ACTH) and correlated to ACTH-responsiveness of both COX2 and AKR1B7/B1. The pivotal role of AKR1B7 in ACTH-induced PGF 2α  release and functional coupling with COX2 was demonstrated using over- and down-expression in cell lines. PGF 2α  receptor was only detected in chromaffin cells, making  medulla  the primary target of PGF 2α  action. By comparing PGF 2α -responsiveness of isolated cells and whole adrenal cultures, we demonstrated that PGF 2α  repressed glucocorticoid secretion by an indirect mechanism involving a decrease in catecholamine release which in turn decreased adrenal steroidogenesis. PGF 2α  may be regarded as a negative autocrine/paracrine regulator within a novel intra-adrenal feedback loop. The coordinated cell-specific regulation of COX2 and AKR1B7 ensures the generation of this stress-induced corticostatic signal.

Aldo Keto Reductase 1B7 and Prostaglandin F2α Are Regulators of Adrenal Endocrine Functions