期刊
JOURNAL OF ANDROLOGY
卷 31, 期 4, 页码 365-371出版社
AMER SOC ANDROLOGY, INC
DOI: 10.2164/jandrol.109.009019
关键词
Dexamethasone; glucocorticoid receptor; steroidogenesis; progenitor Leydig cells
类别
资金
- NIH [RO1 HD050570]
Glucocorticoid (GC) inhibits testosterone production in adult Leydig cells by the glucocorticoid receptor (GR). However, whether GC affects the development of Leydig cells is unclear. The goal of the present study is to investigate the effects of GC on steroidogenesis of rat progenitor Leydig cells (PLCs) in vitro. Dexamethasone (DEX) inhibited androsterone (AO) production in PLCs. The GR antagonist RU38486 reversed the DEX-induced inhibition of AO, whereas the mineralocorticoid receptor antagonist RU28318 did not. RU38486 also reversed DEX-induced reductions in steady-state mRNA levels of steroidogenic acute regulatory protein (Star) and 3 beta-hydroxysteroid dehydrogenase 1 (Hsd3b1). Steroidogenic acute regulatory protein (StAR) protein expression and 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) enzyme activity were affected similarly. These results show that GCs inhibit steroidogenesis of PLCs by suppression of StAR and 3 beta HSD via a GR-mediated mechanism.
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