Enhanced glucocorticoid exposure facilitates the expression of genes involved in prostaglandin and estrogen syntheses in bovine placentomes at induced parturition.

The mechanism by which the fetal membrane detaches after parturition in cattle is poorly understood, but the upregulation of placentomal prostaglandin and estrogen synthesis are considered to be important. This study investigated whether enhanced glucocorticoid exposure affected the functional maturation of placentomes at induced parturition. Placentomes were collected immediately after spontaneous (beef; n = 5, dairy; n = 5) or induced parturition in beef and dairy cattle. Parturition was induced conventionally using prostaglandin F2α (beef; n = 7, dairy; n = 6) or dexamethasone (beef; n = 6) or with a combination of triamcinolone acetonide (a long-acting glucocorticoid) and a high dose of betamethasone (TABET treatment, beef; n = 6, dairy; n = 9). Gene expression levels and protein localization in placentomes were analyzed by RT-qPCR and immunohistochemistry, respectively. Compared with the conventional methods, TABET treatment resulted in upregulated PTGS2 expression in cotyledons. The expression levels of PTGS2 and PGES were positively correlated in both cotyledons and caruncles. TABET treatment also upregulated the expression of CYP17A1, but not of CYP19A1, in cotyledons. The results revealed, for the first time, that PLA2G4A was localized in microvascular endothelial cells in the cotyledonary villi and the maternal septum. PTGS2 and PGES were colocalized in mononucleated cells of the cotyledonary villi and caruncle epithelial cells adjacent to the chorionic plate. TABET treatment upregulated the expression of placentomal genes involved in PGE2 synthesis and the conversion of pregnenolone to androstenedione. Thus, enhanced glucocorticoid exposure might partially facilitate the functional maturation of placentomes at induced parturition in cattle.