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Gonadotropin subunit messenger rna concentrations after blockade of gonadotropin releasing hormone action testosterone selectively increases fsh beta subunit messenger rna by posttranscriptional mechanisms


, : Gonadotropin subunit messenger rna concentrations after blockade of gonadotropin releasing hormone action testosterone selectively increases fsh beta subunit messenger rna by posttranscriptional mechanisms. Molecular Endocrinology 4(12): 1943-1955

Regulation of gonadotropin gene expression by sex steroids may occur via direct effects on the pituitary and/or indirect effects of steroids mediated through hypothalamic GnRH. We aimed to define the effects of testosterone (T) on .alpha., LH.beta., and FSH.beta. mRNA expression in the male rat after blockade of GnRH action on the gonadotrope. A water-soluble GnRH antagonist was administered iv to castrate male rats (increased endogenous GnRH secretion) and to castrate T-replaced rats in which gonadotropin subunit mRNAs had been increased by prior treatment with exogenous GnRH pulses. In castrate male rats, GnRH antagonist resulted in a fall in all three subunit mRNAs. Alpha and LH.beta. declined at slower rates (half-disappearance after 50 and 65 h, respectively) and neither fell to values present in intact rats over 84 h. In contrast, FSH.beta. mRNA declined more rapidly, with a half-disappearance after 20 h. In castrate T replaced rats, .alpha. mRNA declined at a rate similar to that in castrates (half-disappearance after 50 h). LH.beta. declined more slowly, and the rate of FSH.beta. decline was markedly prolonged in the presence of T (half-disappearance time increased from 20 to 50 h). These results suggest that T exerts direct effects on FSH.beta. transcription or mRNA stability which are independent of GnRH action. To assess these possibilities, a long-acting gnRH antagonist (Detirelix) was administered to castrate male rats, which also received T or sham implants 4 days after castration. FSH.beta. mRNA levels fell during the 4 days of Detirelix alone, but the addition of T on day 4 resulted in 2-fold rise in FSH.beta. mRNA, restoring FHS.beta. mRNA to levels present in intact rats. Serum FSH closely paralleled FSH.beta. mRNA concentrations. Alpha mRNA was reduced by 25%, and LH.beta. mRNA concentrations were unchanged in the presence of T. The rate of .alpha. mRNA transcription was markedly reduced and that of LH.beta. tended to fall in T-treated rats, but T had no significant effect on the FSH.beta. transcription rate. Thus, the action of T to increase concentrations of cystolic FSH.beta. mRNA appears to be exerted at a posttranscriptional level, possibly via effects of T on FSH.beta. mRNA stability. This may represent a mechanism by which T can effect differential regulation of gonadotropin subunit mRNA concentrations.

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