Gonadotrophin-releasing hormone-I and -II stimulate steroidogenesis in prepubertal murine Leydig cells in vitro.
- Author:
Yung-Ming LIN
1
;
Ming-Yie LIU
;
Song-Ling POON
;
Sew-Fen LEU
;
Bu-Miin HUANG
Author Information
- Publication Type:Journal Article
- MeSH: 3-Hydroxysteroid Dehydrogenases; biosynthesis; genetics; Animals; Blotting, Western; Cell Separation; Cells, Cultured; Cholesterol Side-Chain Cleavage Enzyme; biosynthesis; Dose-Response Relationship, Drug; Gonadotropin-Releasing Hormone; agonists; pharmacology; Leydig Cells; drug effects; metabolism; Male; Mice; Mice, Inbred C57BL; Phosphoproteins; biosynthesis; genetics; RNA; biosynthesis; isolation & purification; Reverse Transcriptase Polymerase Chain Reaction; Sexual Maturation; physiology; Steroids; biosynthesis; Testosterone; biosynthesis
- From: Asian Journal of Andrology 2008;10(6):929-936
- CountryChina
- Language:English
-
Abstract:
AIMTo study the effect and mechanism of gonadotrophin-releasing hormone (GnRH) on murine Leydig cell steroidogenesis.
METHODSPurified murine Leydig cells were treated with GnRH-I and -II agonists, and testosterone production and steroidogenic enzyme expressions were determined.
RESULTSGnRH-I and -II agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner (P < 0.05). The mRNA expressions of steroidogenic acute regulatory (StAR) protein, P450scc, 3beta-hydroxysteroid dehydrogenase (HSD), but not 17alpha-hydroxylase or 17beta-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase (P < 0.05). However, only 3beta-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase (P < 0.05).
CONCLUSIONGnRH directly stimulated murine Leydig cell steroidogenesis by activating 3b-HSD enzyme expression.