Regulation of Transforming Growth Factor-β-Receptor Type I and Type II Messenger Ribonucleic Acid Expression in the Hamster Ovary by Gonadotropinsand Steroid Hormones1

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Abstract
The hormonal regulation of ovarian transforming growth factor-β (TGF-β) type I receptor (TβRI) and TβRII messenger (mRNA) expression was evaluated using cyclic and hypophysectomized hamsters. Northern blot analysis revealed that three TβRI and one TβRII 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 TβRI mRNA levels recovered partially by 1500 h to fall again by 1600 h. Although hypophysectomy preferentially reduced TβRII mRNA levels, gonadotropins as well as ovarian steroids significantly induced TβRI and TβRII mRNA expression within 48 h and 24 h, respectively; 5α-dihydrotesterone (DHT) induced only TβRII mRNA. The induction of ovarian TβRI and TβRII mRNA by estradiol-17β 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-β 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.

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