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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.