title: Stimulation of c-jun and c-myb in rat Sertoli cells following exposure to retinoids.
abstract: Circulating hormones are engaged in initiating and controlling the process of spermatogenesis, however, the Sertoli cell tight junctions prevent these substances from directly influencing the spermatogenic cells. Thus, the Sertoli cells play a vital role in regulating the spermatogenic process. Our studies correlate retinoid action with the transactivation of genes which encode the transcription factors, Jun and Myb, in the Sertoli cells of the rat testis, a retinol-dependent organ. We examined the mRNA levels for the protooncogene, c-jun, a member of the AP-I transcription complex, as well as mRNA levels for the protooncogene, c-myb, following retinoid stimulation. The major changes observed were a significant up-regulation in c-jun mRNA beginning at 30 min which reached a four-fold peak over controls at 1 h while the c-myb mRNA level exhibited a delay in up-regulation which rose abruptly to a significant three-fold peak over controls at 1 h. Interestingly, a variation in transcript size for c-jun (5.4 kb) was also detected in rat Sertoli cells. The significant 50% rise in the c-jun mRNA levels at 30 min prior to the rapid rise in the c-myb message at 1 h suggests that Jun may be involved in the transactivation of c-myb gene expression. These data support the model that retinoid modulation of these immediate early genes is the first step in a process which initiates a cascade of vitamin A-inducible gene expression in rat Sertoli cells necessary for maintaining spermatogenesis.
authors.affiliation: Biology Department, Bucknell University, Lewisburg, Pennsylvania 17837, USA.
authors.forename: K C
authors.initials: KC
authors.lastname: Page
authors.forename: D A
authors.initials: DA
authors.lastname: Heitzman
authors.forename: M I
authors.initials: MI
authors.lastname: Chernin
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D016758:Genes, jun / Q000187:drug effects*; D006854:Hydrocortisone / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009857:Oncogenes / Q000187:drug effects*; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis; D016755:Proto-Oncogene Proteins c-jun / Q000096:biosynthesis; D020598:Proto-Oncogene Proteins c-myb; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012176:Retinoids / Q000494:pharmacology*; D012708:Sertoli Cells / Q000187:drug effects / Q000378:metabolism*; D013091:Spermatogenesis; D015534:Trans-Activators / Q000096:biosynthesis; D014158:Transcription, Genetic / Q000187:drug effects*; D014168:Transferrin / Q000494:pharmacology; D014212:Tretinoin / Q000494:pharmacology; D014801:Vitamin A / Q000494:pharmacology
chemical_list: D011518:Proto-Oncogene Proteins; D016755:Proto-Oncogene Proteins c-jun; D020598:Proto-Oncogene Proteins c-myb; D012333:RNA, Messenger; D012176:Retinoids; D015534:Trans-Activators; D014168:Transferrin; D014801:Vitamin A; D014212:Tretinoin; D004815:Epidermal Growth Factor; D005640:Follicle Stimulating Hormone; D006854:Hydrocortisone