The prostaglandin E(2) receptor PTGER2 and prostaglandin F(2α) receptor PTGFR mediate oviductal glycoprotein 1 expression in bovine oviductal epithelial cells

Oviductal glycoprotein 1 (OVGP1), an oviductin, is involved in the maintenance of sperm viability and motility and contributes to sperm capacitation in the oviduct. In this study, the regulatory effects exerted by prostaglandin E(2) (PGE(2)) and F(2α) (PGF(2α)) on OVGP1 expression via their corresponding receptors in bovine oviductal epithelial cells (BOECs) were investigated. BOECs were cultured in vitro, and their expression of receptors of PGE(2) (PTGER1, PTGER2, PTGER3, and PTGER4) and PGF(2α) (PTGFR) was measured using RT-qPCR. Ca(2+) concentration was determined with a fluorescence-based method and cAMP was quantified by enzyme-linked immunosorbent assays to verify activation of PTGER2 and PTGFR by their corresponding agonists in these cells. OVGP1 mRNA and protein expression was measured using RT-qPCR and western blotting, respectively, following PTGER2 and PTGFR agonist-induced activation. PTGER1, PTGER2, PTGER4, and PTGFR were found to be present in BOECs; however, PTGER3 expression was not detected. OVGP1 expression was significantly promoted by 10(–6) M butaprost (a PTGER2 agonist) and decreased by 10(–6) M fluprostenol (a PTGFR agonist). In addition, 3 μM H-89 (a PKA inhibitor) and 3 μM U0126 (an ERK inhibitor) effectively inhibited PGE(2)-induced upregulation of OVGP1, and 5 μM chelerythrine chloride (a PKC inhibitor) and 3 μM U0126 negated OVGP1 downregulation by PGF(2α). In conclusion, this study demonstrates that OVGP1 expression in BOECs is enhanced by PGE(2) via PTGER2-cAMP-PKA signaling, and reduced by PGF(2α) through the PTGFR-Ca(2+)-PKC pathway.