Ovarian steroids modulate tumor necrosis factor-α and nitric oxide-regulated prostaglandin secretion by cultured bovine oviductal epithelial cells

Ovarian steroids assure an optimum environment for the final maturation of oocytes, gamete transport, fertilization, and early embryonic development. The aim of experiment I was to examine the influence of ovarian steroids on tumor necrosis factor-a (TNF-alpha) or nitric oxide (NO) regulated prostaglandin (PG), and nitrite/nitrate (NO2/NO3) secretion by cultured bovine oviductal epithelial cells (BOECs). BOECs were pretreated with 17 beta-estradiol (E-2; 10(-9) M) and/or progesterone (P-4; 10(-7) M) for 24 h. For the next 24 h, BOECs were treated with TNF-alpha (10 ng/mL) or spermine nitric oxide complex (NONOate; 10(-5) M). Prostaglandin F-2 alpha and PGE(2) secretion was measured in medium by ELISA. The pretreatment of cells with P-4 (progesterone), E-2 (17 beta-estradiol), or E-2/P-4 augmented TNF-alpha induced PGF(2 alpha) and PGE(2) secretion (P < 0.01). The pretreatment of cells with E-2 or E-2/P-4 increased NONOate-induced PGF(2 alpha) and PGE(2) secretion (P < 0.01). TNF-alpha induced NO2/NO5 production by BOECs. The pretreatment of cells with E-2 augmented only TNF-alpha induced NO2/NO3 production (P < 0.05). The aim of experiment 2 was to examine the influence of TNF-alpha, NO, and ovarian steroids on the protein content of enzymes specifically involved in PG and NO production, PG synthases, and NO synthases (NOSs). BOECs were treated with TNF-alpha (10 ng/mL) or NONOate (10(-5) M). TNF-alpha increased the protein content of PGG/H synthase, PGF synthase, and PGE synthase (P < 0.05) and endothelial and inducible NOSs (P < 0.05). Nitric oxide increased the protein content of PGF synthase, PGE synthase, endothelial NOS, and inducible NOS (P < 0.05). These results show possible linkage between TNF-alpha and NO, modulated by ovarian steroids, in the regulation of PG synthesis by BOECs that may be important for triggering the process of oviductal contractions. (C) 2011 Elsevier Inc. All rights reserved.