Growth hormone regulates steroidogenic acute regulatory protein expression and steroidogenesis in Leydig cell progenitors (PDF)
Kanzaki,Masanori; Morris,Patricia L.
Endocrinology 140(4): 1681-1686
Publication date: 1999
Gonadal development and differentiation is dependent in parton GH, as GH deficiency has been implicated as a cause of loweredfertility and spermatogenic cessation in humans and some biologicalmodels. In this study, we demonstrate that GH receptor messengerRNA (mRNA) is preferentially expressed in progenitor Leydigcells (PLCs) isolated and purified from 21-day-old rats. GHinduces significant increases in the levels of steroidogenicacute regulatory protein (StAR), 3ß-hydroxysteroid dehydrogenase(3ß-HSD) expression, and androgen production in PLCs.Additionally, the cytokine interferon- (IFN) markedly inhibitsGH-stimulated StAR mRNA and protein levels. When cells are culturedwith both GH and IFN, IFN decreases the stimulating effect ofGH on androgen production. Treatment of PLCs with cycloheximidedoes not prevent the GH-induced StAR mRNA, indicating that GHinduction of StAR transcripts does not require de novo proteinsynthesis. In contrast, the induction of 3ß-HSD mRNA byGH is altered by cycloheximide treatment. H7, a serine/threoninekinase inhibitor, completely abrogates the increases in StARmRNA by GH, whereas the tyrosine kinase inhibitor genistein doesnot. Moreover, GH further enhances StAR and 3ß-HSD mRNA expressionin isolated adult rat Leydig cells despite their increased basalexpression subsequent to maturational acquisition of these steroidogeniccomponents. These data provide the first demonstration of thedirect effects of GH on testicular steroidogenesis during progenitorLeydig cell differentiation.
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