Related Experiment Video

Updated: Aug 9, 2026

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
07:22

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells

Published on: March 28, 2013

Differential implication of StAR and P450c17 in TGFbeta1-induced decrease of adrenocortical steroidogenesis

C Brand1, S Bailly, G Defaye

  • 1INSERM Unit 244, Department of Molecular and Structural Biology, CEA/G, Grenoble, France.

Endocrine Research
|January 15, 1999
PubMed

Insights

Transforming growth factor beta 1 (TGFbeta1) affects steroidogenic acute regulatory protein (StAR) and P450c17 expression in bovine adrenocortical cells. StAR appears to be the primary in vivo target of TGFbeta1 in the adrenal cortex.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Adrenocortical fasciculata cells dedifferentiate in primary culture.
  • Transforming growth factor beta (TGFbeta) has known targets in these cells: StAR and P450c17.

Purpose of the Study:

  • Investigate TGFbeta1 regulation of StAR and P450c17 expression over time in primary cell culture.
  • Determine the primary in vivo target of TGFbeta1 in the adrenal cortex.

Main Methods:

  • Primary culture of bovine adrenocortical fasciculata cells.
  • Treatment with TGFbeta1 and ACTH at different time points (Day 1 and Day 4).
  • Analysis of StAR and P450c17 mRNA expression levels.

Main Results:

  • On Day 1, TGFbeta1 decreased basal StAR and P450c17 expression. In the presence of ACTH, TGFbeta1 down-regulated StAR but not P450c17 mRNA.
  • On Day 4, TGFbeta1 down-regulated both StAR and P450c17 mRNA in the absence and presence of ACTH.
  • These time-dependent effects suggest differential regulation of these genes by TGFbeta1.

Conclusions:

  • TGFbeta1 exhibits time-dependent regulation of StAR and P450c17 expression in cultured bovine adrenocortical cells.
  • StAR is identified as the most likely major in vivo target of TGFbeta1 action within the adrenal cortex.

More Related Videos

Isolation, Fixation, and Immunofluorescence Imaging of Mouse Adrenal Glands08:37

Isolation, Fixation, and Immunofluorescence Imaging of Mouse Adrenal Glands

Published on: October 2, 2018

Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions04:33

Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions

Published on: March 12, 2019

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...