Author(s): Liang Chen~1 Zhong-Cheng Xin~1 Xin Li~2 Long Tian~1 Yi-Ming Yuan~1 Gang Liu~1 Xue-Jun Jiang~3 Ying-Lu Guo~11 Andrology Center of Peking University First Hospital, Beijing 100009, China2 Department of Surgery, People's Hospital of Zhangqiu, Zhangqiu 250200, China3 Institute of Microbiology, Chinese Academy of Sciences, Beijing 100080, China
Pages: 589-594
Year: 2006 Issue:  5
Journal: Asian Journal of Andrology
Keyword:  GetLinkList(KeywordFilter('Cox7a2; fusion protein; steroidogenesis; steroidogenic acute regulatory protein; reactive oxygen species; Leydig cell'); 'kw'; 'CJFQ');
Abstract: <正> Aim:To investigate the regulatory function of Cox7a2 on steroidogenesis and the mechanism involved in TM3 mouseLeydig cells.Methods:The cDNA of CoxTa2 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 byWestern blot and fluorometer,respectively.Results:The cDNA of Cox7a2(249 bp)was cloned from Leydig cells andconfirmed by DNA sequencing.After constructed pDsRed-Express-N1-Cox7a2 was transfected back into TM3 mouseLeydig cells,Cox7a2 inhibited not only luteinizing hormone(LH)-induced secretion of testosterone but also the expres-sion 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,byincreasing ROS activity in TM3 mouse Leydig cells.(Asian J Androl 2006 Sep;8:589-594)