title: The role of glucocorticoid in the regulation of prostaglandin biosynthesis in non-pregnant bovine endometrium.
abstract: To determine whether glucocorticoids (GCs) play a role in regulating uterine function in cow, the present study examined the expression of mRNA encoding GC receptor (GC-R) alpha, 11beta-hydroxysteroid dehydrogenase (11-HSD) type 1 and type 2, and the activity of 11-HSD1 in bovine endometrial tissue throughout the estrous cycle. We also studied the effects of cortisol on basal, oxytocin (OT)- and tumor necrosis factor-alpha (TNFalpha)-stimulated prostaglandin (PG) production. A quantitative real-time PCR analysis revealed that GC-Ralpha mRNA was expressed more strongly in the mid-luteal stage (days 8-12) than in the other stages. In contrast to GC-Ralpha mRNA expression, 11-HSD1 mRNA expression was greater in the follicular stage than in the other stages, whereas 11-HSD2 mRNA expression was lowest in the follicular stage. The activity of 11-HSD1 was greater in the follicular stage and estrus than in the other stages and was lowest in the mid-luteal stage. Cortisone was dose-dependently converted to cortisol in the cultured endometrial tissue. Although cortisol did not affect either the basal or OT-stimulated production of PGs in the cultured epithelial cells, the production of PGs stimulated by TNFalpha in the stromal cells was suppressed by cortisol (P < 0.05). Cortisol suppressed basal prostaglandin (PG)F2alpha without affecting basal PGE2 production in the stromal cells. The overall results suggest that the level of cortisol is locally regulated in bovine endometrium throughout the estrous cycle by 11-HSD1, and that cortisol could act as a luteoprotective factor by selectively suppressing luteolytic PGF2alpha production in bovine endometrium.
authors.affiliation: Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
authors.forename: Hwa-Yong
authors.initials: HY
authors.lastname: Lee
authors.forename: Tomas J
authors.initials: TJ
authors.lastname: Acosta
authors.forename: Michiyo
authors.initials: M
authors.lastname: Tanikawa
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Sakumoto
authors.forename: Junichi
authors.initials: J
authors.lastname: Komiyama
authors.forename: Yukari
authors.initials: Y
authors.lastname: Tasaki
authors.forename: Mariusz
authors.initials: M
authors.lastname: Piskula
authors.forename: Dariusz J
authors.initials: DJ
authors.lastname: Skarzynski
authors.forename: Masafumi
authors.initials: M
authors.lastname: Tetsuka
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Okuda
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000235:genetics; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000235:genetics; D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D003348:Cortisone / Q000378:metabolism; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004717:Endometrium / Q000378:metabolism*; D004971:Estrus / Q000378:metabolism*; D005260:Female; D006854:Hydrocortisone / Q000502:physiology*; D010121:Oxytocin / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000032:analysis; D011965:Receptors, Glucocorticoid / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013268:Stimulation, Chemical; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D011453:Prostaglandins; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D014409:Tumor Necrosis Factor-alpha; C411470:glucocorticoid receptor alpha; D010121:Oxytocin; D015237:Dinoprost; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2; D015232:Dinoprostone; D003348:Cortisone; D006854:Hydrocortisone