title: Progesterone stimulates expression of follistatin splice variants Fst288 and Fst315 in the mouse uterus.
abstract: Follistatin, an inhibitor of activin A, has key regulatory roles in the female reproductive tract. Follistatin has two splice variants: FST288, largely associated with cell surfaces, and FST315, the predominant circulating form. The mechanism regulating uterine expression of these variants is unknown. Quantitative RT-PCR was used to measure expression of follistatin splice variants (Fst288, Fst315), the activin bA subunit (Inhba) and the inhibin a subunit (Inha) in uterine tissues during early pregnancy (days 1–4, preimplantation) and in response to exogenous 17b-oestradiol (single s.c. injection) and progesterone (three daily s.c. injections) in ovariectomized mice. Uterine Fst288, Fst315 and Inhba expression increased during early pregnancy, with greater increases in Fst315 relative to Fst288 suggesting differential regulation of these variants. Fst288, Fst315, Inhba and Inha all increased in response to progesterone treatment. Fst288, but not Fst315, mRNA decreased in response to 17b-oestradiol treatment, whereas Inhba increased. A comparison of the absolute concentrations of uterine follistatin mRNA using crossing thresholds indicated that both variants were more highly expressed in early pregnancy in contrast to the hormone treatment models. It is concluded that progesterone regulates uterine expression of both follistatin variants, as well as activin A, during early pregnancy in the mouse uterus
authors.affiliation: Centre for Women's Health Research, Monash University Department of Obstetrics and Gynaecology, Monash Institute of Medical Research, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia.
authors.forename: R G
authors.initials: RG
authors.lastname: Craythorn
authors.forename: W R
authors.initials: WR
authors.lastname: Winnall
authors.forename: F
authors.initials: F
authors.lastname: Lederman
authors.forename: E J
authors.initials: EJ
authors.lastname: Gold
authors.forename: A E
authors.initials: AE
authors.lastname: O'Connor
authors.forename: D M
authors.initials: DM
authors.lastname: de Kretser
authors.forename: M P
authors.initials: MP
authors.lastname: Hedger
authors.forename: P A W
authors.initials: PA
authors.lastname: Rogers
authors.forename: J E
authors.initials: JE
authors.lastname: Girling
mesh_terms: D000818:Animals; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D038681:Follistatin / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects*; D028322:Inhibin-beta Subunits / Q000235:genetics / Q000378:metabolism; D007265:Inhibins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D011247:Pregnancy; D011374:Progesterone / Q000494:pharmacology*; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D014599:Uterus / Q000187:drug effects* / Q000378:metabolism
chemical_list: D038681:Follistatin; D020033:Protein Isoforms; D012333:RNA, Messenger; C103008:inhibin beta A subunit; C094377:inhibin-alpha subunit; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D028322:Inhibin-beta Subunits