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Abstract

Volume 8, Issue 5 (September 2006) 8, 589–594; 10.1111/j.1745-7262.2006.00178.x

Cox7a2 mediates steroidogenesis in TM3 mouse Leydig cells

Liang Chen, Zhong-Cheng Xin, Xin Li, Long Tian, Yi-Ming Yuan, Gang Liu, Xue-Jun Jiang and Ying-Lu Guo

1.Andrology Center of Peking University First Hospital, Beijing 100009, China
2.Department of Surgery, People's Hospital of Zhangqiu, Zhangqiu 250200, China
3.Institute of Microbiology, Chinese Academy of Sciences, Beijing 100080, China

Correspondence: Dr Zhong-Cheng Xin, Andrology Center of Peking University First Hospital, Beijing 100009, China. Fax: +86-10-6618-2822. E-mail: xinzc@bjmu.edu.cn

Received 31 October 2005; Accepted 18 March 2006.

Abstract

Aim: To investigate the regulatory function of Cox7a2 on steroidogenesis and the mechanism involved in TM3 mouse Leydig cells.

Methods: The cDNA of Cox7a2 was cloned from TM3 mouse Leydig cells. It was subcloned to pDsRed-Express-N1 and transfected back into TM3 mouse Leydig cells for Cox7a2 overexpression by transient gene transfection. Steroidogenesis affected by overexpressed Cox7a2 was studied by ELISA. To elicit the mechanism of this effect, expression of steroidogenic acute regulatory (StAR) protein and reactive oxygen species (ROS) were examined by Western blot and fluorometer, respectively.

Results: The cDNA of Cox7a2 (249 bp) was cloned from Leydig cells and confirmed by DNA sequencing. After constructed pDsRed-Express-N1-Cox7a2 was transfected back into TM3 mouse Leydig cells, Cox7a2 inhibited not only luteinizing hormone (LH)-induced secretion of testosterone but also the expression of StAR protein. At the same time, Cox7a2 increased the activity of ROS in TM3 mouse Leydig cells.

Conclusion: Cox7a2 inhibited LH-induced StAR protein expression, and consequent testosterone production, at least in part, by increasing ROS activity in TM3 mouse Leydig cells.

Keywords: Cox7a2, fusion protein, steroidogenesis, steroidogenic acute regulatory protein, reactive oxygen species, Leydig cell

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Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.