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Glucocorticoid receptor functions in HeLa Cells are perturbed by 2,3,8,9-tetrachlorodibenzo-p-dioxin (TCDD)
R. Vrzal, J. Ulrichová, Z. Dvořák, P. Pávek
Drug metabolism letters.
2007 ;
1 (4) :
311-314.
Language English Country United Arab Emirates
Persistent link
https://www.medvik.cz/link/bmc11010042
- MeSH
- Dexamethasone pharmacology MeSH
- Down-Regulation drug effects MeSH
- Financing, Organized MeSH
- Glucocorticoids pharmacology MeSH
- HeLa Cells MeSH
- Environmental Pollutants toxicity MeSH
- Humans MeSH
- RNA, Messenger metabolism drug effects MeSH
- Uterine Cervical Neoplasms metabolism MeSH
- Polychlorinated Dibenzodioxins toxicity MeSH
- Receptors, Aryl Hydrocarbon metabolism drug effects MeSH
- Receptors, Glucocorticoid metabolism drug effects MeSH
- Check Tag
- Humans MeSH
- Female MeSH
We used 2,3,8,9-tetrachlorodibenzo-p-dioxin (TCDD) and dexamethasone (DEX) to examine their effects on aryl hydrocarbon receptor (AhR) and glucocorticoid receptor (GR) in HeLa cells. TCDD (5 nM), DEX (100 nM) and their combination down-regulated GR after 24 h. DEX reversed AhR mRNA increase and AhR protein decrease caused by TCDD. Since AhR-GR cross-talk occurs in cell-type and species-specific manner, the presented data may serve as the basis in the understanding of mechanisms underlying mutual interactions between AhR and GR.
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