Development and function of the adult generation of Leydig cells in mice with sertoli cell-selective or total ablation of the androgen receptor

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dc.contributor.authorDe Gendt, K.
dc.contributor.authorAtanassova, N.
dc.contributor.authorTan, K.
dc.contributor.authorde Franca, L.
dc.contributor.authorParreira, G.
dc.contributor.authorMcKinnell, C.
dc.contributor.authorSharpe, R.
dc.contributor.authorSaunders, P.
dc.contributor.authorMason, J.
dc.contributor.authorHartung, S.
dc.contributor.authorIvell, R.
dc.contributor.authorDenolet, E.
dc.contributor.authorVerhoeven, G.
dc.date.issued2005
dc.description.abstractIt is established that androgens and unidentified Sertoli cell (SC)-derived factors can influence the development of adult Leydig cells (LC) in rodents, but the mechanisms are unclear. We evaluated adult LC development and function in SC-selective androgen receptor (AR) knockout (SCARKO) and complete AR knockout (ARKO) mice. In controls, LC number increased 26-fold and LC size increased by approximately 2-fold between 12 and 140 d of age. LC number in SCARKOs was normal on d 12, but was reduced by more than 40% at later ages, although LC were larger and contained more lipid droplets and mitochondria than control LC by adulthood. ARKO LC number was reduced by up to 83% at all ages compared with controls, and LC size did not increase beyond d 12. Serum LH and testosterone levels and seminal vesicle weights were comparable in adult SCARKOs and controls, whereas LH levels were elevated 8-fold in ARKOs, although testosterone levels appeared normal. Immunohistochemistry and quantitative PCR for LC-specific markers indicated steroidogenic function per LC was probably increased in SCARKOs and reduced in ARKOs. In SCARKOs, insulin-like factor-3 and estrogen sulfotransferase (EST) mRNA expression were unchanged and increased 3-fold, respectively, compared with controls, whereas the expression of both was reduced more than 90% in ARKOs. Changes in EST expression, coupled with reduced platelet-derived growth factor-A expression, are potential causes of altered LC number and function in SCARKOs. These results show that loss of androgen action on SC has major consequences for LC development, and this could be mediated indirectly via platelet-derived growth factor-A and/or estrogens/EST.
dc.description.statementofresponsibilityKarel De Gendt, Nina Atanassova, Karen A. L. Tan, Luiz Renato de França, Gleydes Gambogi Parreira, Chris McKinnell, Richard M. Sharpe, Philippa T. K. Saunders, J. Ian Mason, Stefan Hartung, Richard Ivell, Evi Denolet, and Guido Verhoeven
dc.identifier.citationEndocrinology, 2005; 146(9):4117-4126
dc.identifier.doi10.1210/en.2005-0300
dc.identifier.issn0013-7227
dc.identifier.issn1945-7170
dc.identifier.urihttp://hdl.handle.net/2440/27544
dc.language.isoen
dc.publisherEndocrine Soc
dc.rights© 2005 by The Endocrine Society
dc.source.urihttps://doi.org/10.1210/en.2005-0300
dc.subjectTestis
dc.subjectLeydig Cells
dc.subjectSertoli Cells
dc.subjectAnimals
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMice
dc.subjectReceptors, Androgen
dc.subjectAndrogens
dc.subjectMicroscopy, Electron
dc.subjectCell Count
dc.subjectAge Factors
dc.subjectFemale
dc.subjectMale
dc.titleDevelopment and function of the adult generation of Leydig cells in mice with sertoli cell-selective or total ablation of the androgen receptor
dc.typeJournal article
pubs.publication-statusPublished

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