Regulation of transforming growth factor-beta-receptor type I and type II messenger ribonucleic acid expression in the hamster ovary by gonadotropins and steroid hormones.
The hormonal regulation of ovarian transforming growth factor-beta (TGF-beta) type I receptor (TbetaRI) and TbetaRII messenger (mRNA) expression was evaluated using cyclic and hypophysectomized hamsters. Northern blot analysis revealed that three TbetaRI and one TbetaRII gene transcripts were expressed in the hamster ovary. Reverse transcription-polymerase chain reaction quantitation revealed that receptor mRNA was differentially expressed during the estrous cycle. Although, mRNA levels for both receptor types increased steadily up to Day 4:0900 h, a sharp decline occurred following the gonadotropin surge. In fact, receptor mRNA started declining by Day 4:1200 h, long before the gonadotropin surge; however, only TbetaRI mRNA levels recovered partially by 1500 h to fall again by 1600 h. Although hypophysectomy preferentially reduced TbetaRII mRNA levels, gonadotropins as well as ovarian steroids significantly induced TbetaRI and TbetaRII mRNA expression within 48 h and 24 h, respectively; 5alpha-dihydrotesterone (DHT) induced only TbetaRII mRNA. The induction of ovarian TbetaRI and TbetaRII mRNA by estradiol-17beta() or progesterone was severely attenuated by dexamethasone. A marked increase in serum cortisol coincided with the periovulatory rise in serum gonadotropins. These results suggest that the increase in TGF-beta receptor mRNA expression correlates with gonadotropin-induced ovarian follicular development during the estrous cycle. Moreover, receptor mRNA expression is critically and differentially regulated by gonadotropins as well as ovarian steroids. Most importantly, glucocorticoid appears to play a critical modulatory role in the temporal expression of receptor mRNA in the ovary, hence, controlling folliculogenesis.
Roy
S K
SK
Leland J. and Dorothy H. Olson Center for Women's Health, Department of Ob/Gyn and Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198-4515, USA. skroy@unmc.edu
D030201:Activin Receptors, Type I; D000818:Animals; D006224:Cricetinae; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects*; D006065:Gonadotropins, Pituitary / Q000494:pharmacology*; D006728:Hormones / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000494:pharmacology; D008647:Mesocricetus; D010053:Ovary / Q000737:chemistry* / Q000187:drug effects; D011374:Progesterone / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction
D006065:Gonadotropins, Pituitary; D006728:Hormones; D012333:RNA, Messenger; D018125:Receptors, Transforming Growth Factor beta; D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D017346:Protein Serine-Threonine Kinases; D030201:Activin Receptors, Type I; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II