Effect of Transforming Growth Factor-β1 on Expression of Aryl Hydrocarbon Receptor and Genes of AhGene Battery: Clues for Independent Down-Regulation in A549 Cells

1997 ◽  
Vol 51 (5) ◽  
pp. 703-710 ◽  
Author(s):  
Olaf Döhr ◽  
Ralf Sinning ◽  
Christoph Vogel ◽  
Peter Münzel ◽  
Josef Abel
Keyword(s):  
Growth Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Transforming Growth Factor ◽  
A549 Cells ◽  
Transforming Growth Factor Β1 ◽  
Down Regulation ◽  
Aryl Hydrocarbon

Cell-Specific Regulation of Human Aryl Hydrocarbon Receptor Expression by Transforming Growth Factor-β1

2001 ◽  
Vol 59 (4) ◽  
pp. 716-724 ◽  
Author(s):  
Sandra Wolff ◽  
Patricia A. Harper ◽  
Judy M. Y. Wong ◽  
Volker Mostert ◽  
Yanping Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Receptor Expression ◽  
Aryl Hydrocarbon ◽  
Specific Regulation

scholarly journals Ligand-Independent Regulation of Transforming Growth Factor β1 Expression and Cell Cycle Progression by the Aryl Hydrocarbon Receptor

2007 ◽  
Vol 27 (17) ◽  
pp. 6127-6139 ◽  
Author(s):  
Xiaoqing Chang ◽  
Yunxia Fan ◽  
Saikumar Karyala ◽  
Sandy Schwemberger ◽  
Craig R. Tomlinson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Aryl Hydrocarbon Receptor ◽  
Rna Binding ◽  
Transforming Growth Factor ◽  
Kinase Inhibitor ◽  
Transforming Growth Factor Β1 ◽  
Cyclin Dependent Kinase ◽  
Aryl Hydrocarbon ◽  
Tgf Β1

ABSTRACT The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the toxic effects of its xenobiotic ligands and acts as an environmental checkpoint during the cell cycle. We expressed stably integrated, Tet-Off-regulated AHR variants in fibroblasts from AHR-null mice to further investigate the AHR role in cell cycle regulation. Ahr +/+ fibroblasts proliferated significantly faster than Ahr − / − fibroblasts did, and exposure to a prototypical AHR ligand or deletion of the ligand-binding domain did not change their proliferation rates, indicating that the AHR function in cell cycle was ligand independent. Growth-promoting genes, such as cyclin and cyclin-dependent kinase genes, were significantly down-regulated in Ahr − / − cells, whereas growth-arresting genes, such as the transforming growth factor β1 (TGF-β1) gene, extracellular matrix (ECM)-related genes, and cyclin-dependent kinase inhibitor genes, were up-regulated. Ahr − / − fibroblasts secreted significantly more TGF-β1 into the culture medium than Ahr +/+ fibroblasts did, and Ahr − / − showed increased levels of activated Smad4 and TGF-β1 mRNA. Inhibition of TGF-β1 signaling by overexpression of Smad7 reversed the proliferative and gene expression phenotype of Ahr − / − fibroblasts. Changes in TGF-β1 mRNA accumulation were due to stabilization resulting from decreased activity of TTP, the tristetraprolin RNA-binding protein responsible for mRNA destabilization through AU-rich motifs. These results show that the Ah receptor possesses interconnected intrinsic cellular functions, such as ECM formation, cell cycle control, and TGF-β1 regulation, that are independent of activation by either exogenous or endogenous ligands and that may play a crucial role during tumorigenesis.

Glucocorticoid-induced down regulation of transforming growth factor-β1 in adult rat lung fibroblasts

Lung ◽  
1995 ◽  
Vol 173 (2) ◽  
pp. 71-78 ◽  
Author(s):  
S. Shull ◽  
N. Meisler ◽  
M. Absher ◽  
S. Phan ◽  
K. Cutroneo
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Lung Fibroblasts ◽  
Rat Lung ◽  
Down Regulation ◽  
Adult Rat
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