Differential Effects of Interferon-τ on the Prostaglandin Synthetic Pathway in Bovine Endometrial Cells Treated with Phorbol Ester

Abstract Rationale for these experiments was to evaluate the dose effects of bovine interferon- τ (IFN- τ ) on the prostaglandin secretory pathway of immortalized bovine endometrial (BEND) cells in response to phorbol 12, 13-dibutyrate (PdBu) and to characterize similar responses in primary bovine uterine epithelial cells as a biomonitor of embryo-induced antiluteolytic effects on the endometrium. The BEND cells were treated with PdBu (0 or 100 ng/mL) and IFN- τ (0 or 50 ng/mL) for 6h. The PdBu stimulated secretions of PGF 2α and prostaglandin E 2 (PGE 2 ). Co-treatment of cells with IFN- τ blocked PdBu-induced secretion of both PGF 2α and PGE 2 . Treatment with PdBu for 6h induced expression of prostaglandin H synthase-2 mRNA, prostaglandin H synthase-2 protein, and prostaglandin E synthase mRNA, which were blocked with concurrent addition of IFN- τ . Doses of IFN- τ (0.05, 0.5, 1, 5, 10, and 20 μ g/mL) were used with PdBu (0 and 100 ng/mL). The IFN- τ alone failed to stimulate secretion of PGF 2α and PGE 2 , whereas IFN- τ doses μ g/mL suppressed PdBu-stimulated secretions of PGF 2α and PGE 2 . Uterine epithelial cells were isolated from cows at d 17 after estrus and were cultured to confluence in serum-free medium. Cells were treated with IFN- τ (0, 50, or 500 ng/mL) and PdBu (0 or 100 ng/mL) before media were collected after 24h for PGF 2α and PGE 2 analyses. Treatment of primary uterine epithelial cells with PdBu induced PGF 2α secretion, and IFN- τ (50 and 500 ng/mL) caused a reduction in PGF 2α secretion induced by PdBu. In the absence of PdBu, IFN- τ increased basal secretion of PGF 2α . Concentrations of PGE 2 increased in response to PdBu, and the 50-ng/mL dose of IFN- τ had a stimulatory effect on PGE 2 concentrations compared with the 500-ng/mL dose in the absence of PdBu. Phorbol ester-induced gene transcription as related to prostaglandin synthesis is regulated by IFN- τ in vitro.