title: Regulation of cyclooxygenase-2 and prostaglandin F synthase gene expression by steroid hormones and interferon-tau in bovine endometrial cells.
abstract: Estradiol (E2) and progesterone are responsible for regulating PG synthesis in the endometrium during the estrous cycle and interferon-tau (IFN-tau) alters PG synthesis during early pregnancy in ruminants. In this study, we examined the effects of these steroid hormones and recombinant bovine IFN-tau (rbIFN-tau) on PG production and on cyclooxygenase-2 (COX-2) and PG F (PGF) synthase (PGFS) gene expression in isolated endometrial cells. E2 decreased both PGF2alpha and PG E2 (PGE2) whereas progesterone increased PGF2alpha secretion in epithelial cells. Steroid hormones had no effect on PG production in stromal cells. rbIFN-tau attenuated both PGF2alpha and PGE2 production in epithelial cells and enhanced their production, and the ratio of PGE2 to PGF2alpha, in stromal cells. Northern blot analysis showed that E2 and rbIFN-tau decreased COX-2 messenger RNA (mRNA) levels in epithelial cells. Conversely, rbIFN-tau increased COX-2 mRNA in stromal cells. Furthermore, rbIFN-tau decreased PGFS mRNA in both cell types and this was associated with the increase in PGE2/PGF2alpha ratio. These results show that the regulation of PG synthesis by steroid hormones is different in endometrial epithelial and stromal cells in vitro. The attenuation of PGF2alpha secretion from epithelial cells and increased PGE2 production in stromal cells by rbIFN-tau are modulated by steroid hormones.
authors.affiliation: Centre de Recherche en Reproduction Animale, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada.
authors.forename: C W
authors.initials: CW
authors.lastname: Xiao
authors.forename: J M
authors.initials: JM
authors.lastname: Liu
authors.forename: J
authors.initials: J
authors.lastname: Sirois
authors.forename: A K
authors.initials: AK
authors.lastname: Goff
mesh_terms: D000818:Animals; D002417:Cattle; D051546:Cyclooxygenase 2; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004717:Endometrium / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D006728:Hormones / Q000494:pharmacology*; D006911:Hydroxyprostaglandin Dehydrogenases / Q000235:genetics*; D007370:Interferon Type I / Q000494:pharmacology*; D007527:Isoenzymes / Q000235:genetics*; D008070:Lipopolysaccharides / Q000494:pharmacology; D011257:Pregnancy Proteins / Q000494:pharmacology*; D011374:Progesterone / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D011994:Recombinant Proteins / Q000494:pharmacology
chemical_list: D006728:Hormones; D007370:Interferon Type I; D007527:Isoenzymes; D008070:Lipopolysaccharides; D011257:Pregnancy Proteins; D012333:RNA, Messenger; D011994:Recombinant Proteins; C020947:interferon tau; D011374:Progesterone; D004958:Estradiol; D015237:Dinoprost; D006911:Hydroxyprostaglandin Dehydrogenases; C031051:prostaglandin-F synthase; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone