Cox7a2 mediates steroidogenesis in TM3 mouse Leydig cells.
- Author:
Liang CHEN
1
;
Zhong-Cheng XIN
;
Xin LI
;
Long TIAN
;
Yi-Ming YUAN
;
Gang LIU
;
Xue-Jun JIANG
;
Ying-Lu GUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Line; Cloning, Molecular; Electron Transport Complex IV; genetics; metabolism; Leydig Cells; drug effects; metabolism; Luteinizing Hormone; pharmacology; Male; Mice; Phosphoproteins; metabolism; Plasmids; Reactive Oxygen Species; metabolism; Recombinant Proteins; metabolism; Testosterone; metabolism; Transfection
- From: Asian Journal of Andrology 2006;8(5):589-594
- CountryChina
- Language:English
-
Abstract:
AIMTo investigate the regulatory function of Cox7a2 on steroidogenesis and the mechanism involved in TM3 mouse Leydig cells.
METHODSThe 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.
RESULTSThe 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.
CONCLUSIONCox7a2 inhibited LH-induced StAR protein expression, and consequent testosterone production, at least in part, by increasing ROS activity in TM3 mouse Leydig cells.
