CONTROLE TRANSCRIPTIONNEL DES ACTIVITES STEROIDOGENES DU CORTEX SURRENAL PAR LE FACTEUR DE TRANSFORMATION TGF-β

Jj, Feige; Cochet, Claude; Pascal, Olivier; Defaye, G.; Perrin, A.; Rainey, Allison; Madani, C.; Chambaz, EM

doi:10.1051/rnd:19890720

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“…Although TGF 1 appears as a strong inhibitor of steroidogenesis in each of these models, the nature of the primary targets down-regulated by this factor greatly differs from one cell type to another and as a function of the metabolic status of a given cell type. In freshly prepared primary cultures of bovine adrenocortical fasciculata cells, we observed that both basal and adrenocorticotropin (ACTH)-induced cortisol production was inhibited by TGF 1 through the down-regulation of steroidogenic acute regulatory protein (StAR) and steroid 17 -hydroxylase (the product of CYP17) expression (Feige et al 1987, Perrin et al 1991, Brand et al 1998b. However, the relative extent of inhibition of these two genes appeared to vary as a function of the age of the primary culture, with CYP17 being less prominently inhibited on day 1 than on day 4 of primary culture in the presence of ACTH (Brand et al 1998a).…”

Section: Introductionmentioning

confidence: 98%

Transforming growth factor beta1 inhibits aldosterone and cortisol production in the human adrenocortical cell line NCI-H295R through inhibition of CYP11B1 and CYP11B2 expression

Liakos¹,

Lenz²,

Bernhardt³

et al. 2003

Journal of Endocrinology

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Transforming growth factor beta1 (TGFbeta1) has been shown to exert strong inhibitory effects on adrenocortical cell steroidogenesis. However, the molecular targets of TGFbeta1 in adrenocortical cells appear to differ between species. Here, we report the first characterization of the regulatory effects of TGFbeta1 on the steroidogenic functions of the human adrenocortical tumor cell line NCI-H295R. After treatment with 2 ng/ml TGFbeta1 for 24 h, basal production of corticosterone, cortisol and androstenedione was dramatically decreased. When TGFbeta1 was added simultaneously with forskolin, the production of cortisol and 11-hydroxyandrostenedione was decreased by 85% whereas that of deoxycortisol was increased. When TGFbeta1 was added simultaneously with angiotensin II, aldosterone production was reduced by 80%. We observed that TGFbeta1 strongly inhibits forskolin-induced steroid 11beta-hydroxylase activity and CYP11B1 mRNA levels, as well as angiotensin II-induced aldosterone synthase activity and CYP11B2 mRNA levels. CYP11B1 and CYP11B2 gene products thus appear as the major steroidogenic enzymes down-regulated by TGFbeta1 in the human adrenocortical tumor cell line NCI-H295R.

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Section: Introductionmentioning

confidence: 98%