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Research ArticleArticle

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

Olaf Döhr, Ralf Sinning, Christoph Vogel, Peter Münzel and Josef Abel
Molecular Pharmacology May 1997, 51 (5) 703-710; DOI: https://doi.org/10.1124/mol.51.5.703
Olaf Döhr
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Abstract

An inhibitory effect on both constitutive and inducible expression of cytochrome P450 isoenzymes has been shown for different cytokines and growth factors. We previously described an inhibition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced CYP1A1 mRNA and enzyme activity by transforming growth factor-β1 (TGF-β1) in human lung cancer A549 cells. In the present study, we report that not only TCDD-induced expression of CYP1A1 but also basal mRNA expression of CYP1A1, CYP1B1, and aryl hydrocarbon receptor (AHR) was down-regulated by TGF-β1 in cells not treated with TCDD. In contrast, mRNA expression of the AHR partner protein Arnt (aryl hydrocarbon receptor nuclear translocator) was not influenced. Furthermore, TCDD-induced expression of CYP1B1 and NMO-1 was inhibited, and the IC50 values of 5–10 pmTGF-β1 were in the same range as observed for inhibition of CYP1A1 and AHR mRNA expression. Transfection studies with a plasmid containing a luciferase reporter gene under control of two dioxin-responsive elements indicate an effect on AHR protein expression. Results of time-course studies revealed a parallel inhibition of AHR and CYP1 mRNA expression, indicating that TGF-β1 is a direct negative regulator of transcription of these genes. The treatment of cells with cycloheximide led to a superinduction of TCDD-induced CYP1A1 and CYP1B1 mRNA expression and abolished the inhibitory effect of TGF-β1 on basal as well as TCDD-induced CYP1 and AHR mRNA expression. TGF-β1seems not to influence the stability of AHR mRNA. The results suggest that TGF-β1 induces rapid transcription and translation of an as-yet-unknown negative regulatory factor or factors that may directly regulate expression of AHR and genes of Ah gene battery.

Footnotes

    • Received October 30, 1996.
    • Accepted January 16, 1997.
  • Send reprint requests to: Dr. Josef Abel, Medical Institute of Environmental Hygiene at the Heinrich-Heine-University of Düsseldorf, Department of Toxicology, Auf’m Hennekamp 50, 40225 Düsseldorf, Germany. E-mail:josef.abel{at}uni-duesseldorf.de

  • This work was supported by Deutsche Forschungsgemeinschaft, Sonderforschungsbereich 503 (DFG-SFB 503/A5)

  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 51 (5)
Molecular Pharmacology
Vol. 51, Issue 5
1 May 1997
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Research ArticleArticle

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

Olaf Döhr, Ralf Sinning, Christoph Vogel, Peter Münzel and Josef Abel
Molecular Pharmacology May 1, 1997, 51 (5) 703-710; DOI: https://doi.org/10.1124/mol.51.5.703

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Research ArticleArticle

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

Olaf Döhr, Ralf Sinning, Christoph Vogel, Peter Münzel and Josef Abel
Molecular Pharmacology May 1, 1997, 51 (5) 703-710; DOI: https://doi.org/10.1124/mol.51.5.703
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