title: Regulation of primary response and specific genes in adrenal cells by peptide hormones and growth factors.
abstract: Using cultured bovine adrenal fasciculata cells (BAC), we investigated the effects of two hormones, corticotropin (ACTH) and angiotensin II (Ang-II) and two growth factors, insulin-like growth factors I (IGF-I) and transforming growth factor beta 1 (TGF beta 1), on the mRNA levels of nuclear proto-oncogenes of the Fos and Jun families and on the mRNA levels of genes expressed in BAC coding for ACTH and AT1 receptors, cytochrome P450scc and P450 17 alpha and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD). ACTH and IGF-1 increased c-fos and jun-B mRNA levels early with later increases in the levels of mRNA for the ACTH receptor and the three steroidogenic enzymes, and enhanced steroidogenic responses to both ACTH and Ang-II. In contrast, Ang-II increased mRNA coding for the three proto-oncogenes (cfos, c-jun, and jun-B), decreased those for P450 17 alpha and 3 beta-HSD, and caused marked homologous and heterologous steroidogenic desensitization. TGF beta 1 increased only jun-B mRNA and markedly reduced BAC-differentiated functions and steroidogenic responsiveness to both ACTH and Ang-II. The long-term effects of ACTH on human adrenal fasciculata cells were comparable with those observed in BAC, whereas the long term effects of Ang-II and TGF beta 1 were different from those observed in BAC. Whether these species-specific differences are related to a different effect of these factors on proto-oncogene expression is not yet known.
authors: INSERM-INRA U418, Hôpital Debrousse, Lyon, France.
authors: A
authors: A
authors: Penhoat
authors: R
authors: R
authors: Ouali
authors: I
authors: I
authors: Viard
authors: D
authors: D
authors: Langlois
authors: J M
authors: JM
authors: Saez
mesh_terms: D000302:Adrenal Cortex / Q000166:cytology / Q000187:drug effects*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002417:Cattle; D002454:Cell Differentiation; D002478:Cells, Cultured; D004351:Drug Resistance; D015972:Gene Expression Regulation, Neoplastic; D006133:Growth Substances / Q000494:pharmacology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology; D000090063:Proto-Oncogene Mas; D011519:Proto-Oncogenes / Q000187:drug effects*; D012333:RNA, Messenger / Q000032:analysis / Q000187:drug effects; D011945:Receptors, Angiotensin / Q000187:drug effects; D018043:Receptors, Corticotropin / Q000187:drug effects; D016212:Transforming Growth Factor beta / Q000494:pharmacology; D015383:Zona Fasciculata / Q000166:cytology / Q000187:drug effects; D015385:Zona Reticularis / Q000166:cytology / Q000187:drug effects
chemical_list: D006133:Growth Substances; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D012333:RNA, Messenger; D011945:Receptors, Angiotensin; D018043:Receptors, Corticotropin; D016212:Transforming Growth Factor beta; D000804:Angiotensin II; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone