Development and Function of the Adult Generation of Leydig Cells in Mice with Sertoli Cell-Selective or Total Ablation of the Androgen Receptor

• DOI: 10.1210/en.2005-0300
• Publication Date: 2005-05-27T00:25:04Z
• Authors: Karel De Gendt; Nina Atanassova; Karen A. L. Tan; Luiz Renato de Fr...; Gleydes Gambogi P...; Chris McKinnell; Richard M. Sharpe; Philippa T. K. Sa...; J. Ian Mason; Stefan Hartung; Richard Ivell; Evi Denolet; Guido Verhoeven
• Keywords: Male; Mice, Knockout; 0301 basic medicine; Microscopy; 0303 health sciences; 571; Sertoli Cells; 572; Knockout; Age Factors; Leydig Cells; Cell Count; Inbred C57BL; Electron; Androgen; Mice, Inbred C57BL; Mice; Microscopy, Electron; 03 medical and health sciences; Receptors, Androgen; Receptors; Testis; Androgens; Animals; Female

Abstract It is established that androgens and unidentified Sertoli cell (SC)-derived factors can influence the development of adult Leydig cells (LC) in rodents, but mechanisms are unclear. We evaluated LC function SC-selective androgen receptor (AR) knockout (SCARKO) complete AR (ARKO) mice. In controls, number increased 26-fold size by approximately 2-fold between 12 140 d age. SCARKOs was normal on 12, reduced more than 40% at later ages, although were larger contained lipid droplets mitochondria control adulthood. ARKO up to 83% all ages compared with did not increase beyond 12. Serum LH testosterone levels seminal vesicle weights comparable whereas elevated 8-fold ARKOs, appeared normal. Immunohistochemistry quantitative PCR for LC-specific markers indicated steroidogenic per probably ARKOs. SCARKOs, insulin-like factor-3 estrogen sulfotransferase (EST) mRNA expression unchanged 3-fold, respectively, both 90% Changes EST expression, coupled platelet-derived growth factor-A potential causes altered SCARKOs. These results show loss action SC has major consequences development, this could be mediated indirectly via and/or estrogens/EST.