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Hepatic vitellogenin (vtg) is a yolk precursor protein sequestered in follicular oocytes as nutrient supply for developing embryos in nonmammalian vertebrates. In prior research studies we have demonstrated that both progesterone (P) and testosterone (T) inhibit estrogen (E)-induced vitellogenesis in the male fresh water turtle (Chrysemys picta), and have suggested that these hormones may be involved in multihormonal regulation of vitellogenesis in the female turtle. However, the modes of action of progesterone and testosterone on estrogen-induced vitellogenesis are not known. We have proposed that progesterone inhibits vitellogenesis by modulation of progesterone receptor A (PRA) or B (PRB) isoforms and/or estrogen receptor (ER) gene transcription. In this study, we compare the vitellogenic responses of reproductively inactive male turtles to estradiol 17b in the presence of exogenous testosterone or progesterone. Northern blot analysis was used to monitor the changes in vtg mRNA, ER mRNA, and PR mRNA expression; Western blotting to determine changes in PR isoform expression and a homologous ELISA for measurement of plasma vtg. Progesterone and testosterone reduced estrogen-induced vtg mRNA expression, but plasma vtg was not significantly reduced by these steroids. PRA and PRB were transcribed even though ER mRNA could not be detected, suggesting constitutive PR expression. However, in the presence of estradiol 17b, both PR isoforms and mRNA transcripts were increased as a correlate of ER mRNA transcription, suggesting both transcriptional and translational effects; these effects were inhibited by testosterone and progesterone treatments. Since ER mRNA was sharply reduced by both testosterone and progesterone, and estradiol 17b increased PR mRNA transcription and translation, it is likely that the action of progesterone in reducing vtg mRNA is indirect via down regulation of ER mRNA, thus ER. This study provides further information on the role of progesterone and testosterone in the regulation of hepatic vitellogenesis, suggesting regulation of vitellogenesis mainly via modulation of hepatic ER mRNA.

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