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Abstract

Volume 10, Issue 6 (November 2008) 10, 929–936; 10.1111/j.1745-7262.2008.00434.x

Gonadotrophin-releasing hormone-I and-II stimulate steroidogenesis in prepubertal murine Leydig cells in vitro

Yung-Ming Lin1, Ming-Yie Liu2, Song-Ling Poon1,3, Sew-Fen Leu4 and Bu-Miin Huang3

1 Department of Urology, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, China
2 Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, China
3 Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan, China
4 Institute of Bioindustrial Technology, College of Human Ecology, HungKuang University, Taichung 43302, Taiwan, China

Correspondence: Dr Bu-Miin Huang, Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, #138, Sheng Li Road, Tainan 70101, Taiwan, China. Fax: +886-2093-007. E-mail: bumiin@mail.ncku.edu.tw

Received 19 December 2007; Accepted 20 April 2008

Abstract

Aim: To study the effect and mechanism of gonadotrophin-releasing hormone (GnRH) on murine Leydig cell steroidogenesis.

Methods: Purified murine Leydig cells were treated with GnRH-I and-II agonists, and testosterone production and steroidogenic enzyme expressions were determined.

Results: GnRH-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, 3β-hydroxysteroid dehydrogenase (HSD), but not 17α-hydroxylase or 17β-HSD, were significantly stimulated by both GnRH agonists with a 1.5-to 3-fold increase (P < 0.05). However, only 3β-HSD protein expression was induced by both GnRH agonists, with a 1.6-to 2-fold increase (P < 0.05).

Conclusion: GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3β-HSD enzyme expression.

Keywords: gonadotrophin-releasing hormone, Leydig cells, murine, steroidogenesis, stimulation

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