Thyroid hormone, retinoic acid, and testosterone suppress proliferation and induce markers of differentiation in cultured rat sertoli cells.
This study uses a high purity cell culture system to extend previous observations of factors controlling the end of the Sertoli cell proliferative phase. Thyroid hormone, retinoic acid, and testosterone were assessed for their ability to halt the proliferative phase and regulate the expression of markers associated with maturation of the Sertoli cell. We show that these hormones share similar suppressive effects on the rate of Sertoli cell division without any apparent additive effects. We demonstrate that these hormones induce the progressive accumulation of cell cycle inhibitors p27Kip1 and p21Cip1 in Sertoli cells, a likely regulatory mechanism controlling the suppression of proliferation. We used real-time RT-PCR to examine the effects of these factors on the expression of mRNA encoding the Id proteins, demonstrating an increase in Id2 and Id3 expression in Sertoli cells treated with thyroid hormone, retinoic acid, or testosterone. Finally, we examined the expression of a number of genes that have been implicated in the Sertoli cell differentiation process. Our results suggest that these hormones can induce aspects of Sertoli cell differentiation in vitro, providing a valuable in vitro model for studying Sertoli cell function.
Buzzard
Jeremy J
JJ
Monash Institute of Reproduction and Development and Department of Anatomy and Cell Biology, Monash University, Clayton, 3168, Melbourne, Australia.
Wreford
Nigel G
NG
Morrison
John R
JR
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D015415:Biomarkers; D018797:Cell Cycle Proteins / Q000235:genetics; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D016213:Cyclins / Q000235:genetics; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D019077:Helix-Turn-Helix Motifs / Q000235:genetics; D066298:In Vitro Techniques; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012708:Sertoli Cells / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D013739:Testosterone / Q000494:pharmacology*; D014212:Tretinoin / Q000494:pharmacology*; D014284:Triiodothyronine / Q000494:pharmacology*; D025521:Tumor Suppressor Proteins / Q000235:genetics
D000970:Antineoplastic Agents; D015415:Biomarkers; C493958:Cdkn1a protein, rat; C493962:Cdkn1b protein, rat; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D012739:Gonadal Steroid Hormones; D012333:RNA, Messenger; D025521:Tumor Suppressor Proteins; D014284:Triiodothyronine; D050760:Cyclin-Dependent Kinase Inhibitor p27; D013739:Testosterone; D014212:Tretinoin; D005640:Follicle Stimulating Hormone