Abstract
BackgroundWe found previously that the expression of SET gene was up-regulated in polycystic ovaries. Evidences suggested that SET protein was essential for regulating both the promoter activity of CYP17A1 and the biological activity of P450c17. In this study, we explored whether SET regulated androgen production in preantral follicles.MethodsThe mouse preantral follicles were cultured in vitro. Testosterone secretion and expression of steroidogenic enzymes were observed in the preantral follicles treated in vitro by SET overexpression and knockdown.ResultsTestosterone levels in the media of the AdCMV-SET infected follicles significantly increased, and the CYP17A1 and HSD3B2 expression also significantly increased (P < 0.05). Testosterone levels in AdSiRNA-SET infected group decreased, and so did CYP17A1 and HSD3B2 expression (P < 0.05).ConclusionsSET played a positive role in regulating ovarian androgen biosynthesis by enhancing the transcription of steroidogenic enzymes CYP17A1 and HSD3B2, which maybe contribute to the hyperandrogenism in PCOS.
Highlights
We found previously that the expression of SET gene was up-regulated in polycystic ovaries
It is well known that theca cells express cytochrome P450 cholesterol sidechain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase (HSD3B2), and cytochrome P450 cytochrome P450 17α-hydroxylase (CYP17A1) which has both 17α-hydroxylase and C17, 20 lyase activities [4]
SET overexpression promoted androgen production in theca cells The in vitro culture model of mouse preantral follicle was used to study the effect of SET on testosterone synthesis in theca cells
Summary
We found previously that the expression of SET gene was up-regulated in polycystic ovaries. The synthesis of androgen in theca cells is regulated by a variety of additional steroidogenic enzymes. It is well known that theca cells express cytochrome P450 cholesterol sidechain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase (HSD3B2), and cytochrome P450 cytochrome P450 17α-hydroxylase (CYP17A1) which has both 17α-hydroxylase and C17, 20 lyase activities [4]. All of these are key enzymes for androgen synthesis. Steroidogenic acute regulatory (StAR) protein which facilitates cholesterol entry into the mitochondria mediates the rate-limiting step in the synthesis of
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