To evaluate the site(s) and mechanism(s) of glucocorticoid-inhibition of transforming growth factor (TGF) β receptor (TβR) mRNA expression in ovarian cells, steady-state levels of TβR mRNA in hamster preantral follicles exposed to FSH or estradiol with or without dexamethasone were determined by reverse transcription polymerase chain reaction and Southern hybridization. The effect of dexamethasone on follicular DNA and steroid synthesis and the expression of NF-Y and Sp3 were also investigated. Dexamethasone differentially inhibited FSH- or estradiol-induced expression of TβR mRNA in preantral follicles at all stages. Dexamethasone also strongly inhibited FSH-induced but not TGFβ2-induced follicular DNA synthesis, and the inhibition was completely reversed by TGFβ2. However, TGFβ2 markedly attenuated FSH dexamethasone-stimulated progesterone and FSH-induced follicular estradiol synthesis. Both FSH and estradiol upregulated NF-YA expression, but the effect was significantly attenuated by dexamethasone. Our results suggest that suppression of NF-YA levels is one of the mechanisms whereby dexamethasone reduces hormone-induced TβRI and TβRII mRNA levels in hamster preantral follicles. Dexamethasone potentiates the effect of FSH on granulosa cell steroidogenesis, whereas TGFβ counteracts the effect. These data indicate that glucocorticoid and TGFβ may form an important regulatory loop to modulate FSH regulation of preantral follicular growth and differentiation.
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