• Media type: E-Article
  • Title: Differentiation-Dependent Expression of 17β-Hydroxysteroid Dehydrogenase, Type 10, in the Rodent Testis: Effect of Aging in Leydig Cells
  • Contributor: Ivell, Richard; Balvers, Marga; Anand, Ravinder J. K.; Paust, Hans-Joachim; McKinnell, Chris; Sharpe, Richard
  • Published: The Endocrine Society, 2003
  • Published in: Endocrinology, 144 (2003) 7, Seite 3130-3137
  • Language: English
  • DOI: 10.1210/en.2002-0082
  • ISSN: 0013-7227; 1945-7170
  • Origination:
  • Footnote:
  • Description: AbstractExpression of the new 17β-hydroxysteroid dehydrogenase (HSD), type 10 (17β-HSD-10), formerly known as endoplasmic reticulum-associated amyloid-binding protein, has been investigated in the testes of various mammals under normal and perturbed conditions. Results show that 17β-HSD-10 is a major product of both fetal and adult-type Leydig cells. In the former, protein persists until late in postnatal development; and in the short-day hamster model, it does not disappear when Leydig cells involute. During puberty in the rat, immunohistochemical staining for 17β-HSD-10 in adult-type Leydig cells first becomes evident on d 20, increasing to maximal staining intensity by d 35. In the rat, but not in the mouse or any other species examined, there is also staining in late spermatids. Examination of testes from rats subjected to perinatal treatment with either a GnRH antagonist or low and high doses of diethylstilbestrol revealed that expression of 17β-HSD-10 follows closely Leydig cell differentiation status, correlating with 3β-HSD expression in a previous study. In aging (23 months) rat testes, Leydig cell (but not germ cell) immunostaining for 17β-HSD-10 is markedly reduced. 17β-HSD-10 seems to preferentially convert 3α-androstanediol into dihydrotestosterone, and estradiol to estrone. Thus, perinatal expression of this enzyme in fetal Leydig cells may contribute to protecting these cells from estrogens and encourage androgen formation.
  • Access State: Open Access