Attributes | Values |
---|
rdf:type
| |
rdfs:seeAlso
| |
Description
| - The JEG-3 choriocarcinoma cell line has been proposed as a model cell line of human placental trophoblast for induction studies via aryl hydrocarbon receptor (AHR). We examined whether glucocorticoid dexamethasone influences AHR-mediated induction of CYP1A1 enzyme in the JEG-3 cell line. We found that dexamethasone dose- and time-dependently suppresses CYP1A1 transactivation in gene reporter assays, CYP1A1 mRNA induction, and upregulation of 7-ethoxyresorufin-O-deethylase (EROD) activity by 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in JEG-3 cells. Co-transfection of JEG-3 cells with glucocorticoid receptor (GR) expression construct and treatment with dexamethasone abolished the effect of MC on CYP1A1 promoter construct in transient transfection gene reporter assays. RU486, a GR antagonist, suppressed the effect of dexamethasone on MC-induced transactivation of AHR responsive reporter constructs. We also found that dexamethasone stimulates both ligand-dependent and ligand-independent degradation of AHR but not of aryl hydrocarbon receptor nuclear translocator (ARNT) protein in JEG-3 cells. In experiments with proteasome inhibitors MG132 and bortezomib, we found that the degradation is not sensitive to proteasome inhibition in JEG-3. We can conclude that dexamethasone suppresses AHR-mediated CYP1A1 induction in JEG-3 cells through the unique mechanism of AHR-GR crosstalk, which involves accelerated degradation of AHR.
- The JEG-3 choriocarcinoma cell line has been proposed as a model cell line of human placental trophoblast for induction studies via aryl hydrocarbon receptor (AHR). We examined whether glucocorticoid dexamethasone influences AHR-mediated induction of CYP1A1 enzyme in the JEG-3 cell line. We found that dexamethasone dose- and time-dependently suppresses CYP1A1 transactivation in gene reporter assays, CYP1A1 mRNA induction, and upregulation of 7-ethoxyresorufin-O-deethylase (EROD) activity by 3-methylcholanthrene (MC) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in JEG-3 cells. Co-transfection of JEG-3 cells with glucocorticoid receptor (GR) expression construct and treatment with dexamethasone abolished the effect of MC on CYP1A1 promoter construct in transient transfection gene reporter assays. RU486, a GR antagonist, suppressed the effect of dexamethasone on MC-induced transactivation of AHR responsive reporter constructs. We also found that dexamethasone stimulates both ligand-dependent and ligand-independent degradation of AHR but not of aryl hydrocarbon receptor nuclear translocator (ARNT) protein in JEG-3 cells. In experiments with proteasome inhibitors MG132 and bortezomib, we found that the degradation is not sensitive to proteasome inhibition in JEG-3. We can conclude that dexamethasone suppresses AHR-mediated CYP1A1 induction in JEG-3 cells through the unique mechanism of AHR-GR crosstalk, which involves accelerated degradation of AHR. (en)
|
Title
| - Dexamethasone accelerates degradation of aryl hydrocarbon receptor (AHR) and suppresses CYP1A1 induction in placental JEG-3 cell line
- Dexamethasone accelerates degradation of aryl hydrocarbon receptor (AHR) and suppresses CYP1A1 induction in placental JEG-3 cell line (en)
|
skos:prefLabel
| - Dexamethasone accelerates degradation of aryl hydrocarbon receptor (AHR) and suppresses CYP1A1 induction in placental JEG-3 cell line
- Dexamethasone accelerates degradation of aryl hydrocarbon receptor (AHR) and suppresses CYP1A1 induction in placental JEG-3 cell line (en)
|
skos:notation
| - RIV/00216208:11160/13:10145995!RIV14-GA0-11160___
|
http://linked.open...avai/riv/aktivita
| |
http://linked.open...avai/riv/aktivity
| - I, P(ED0030/01/01), P(EE2.3.30.0004), P(GAP303/12/0472), P(GBP303/12/G163)
|
http://linked.open...iv/cisloPeriodika
| |
http://linked.open...vai/riv/dodaniDat
| |
http://linked.open...aciTvurceVysledku
| |
http://linked.open.../riv/druhVysledku
| |
http://linked.open...iv/duvernostUdaju
| |
http://linked.open...titaPredkladatele
| |
http://linked.open...dnocenehoVysledku
| |
http://linked.open...ai/riv/idVysledku
| - RIV/00216208:11160/13:10145995
|
http://linked.open...riv/jazykVysledku
| |
http://linked.open.../riv/klicovaSlova
| - Proteasome; MG132; Glucocorticoid receptor; CYP1A1; Choriocarcinoma cell line; Aryl hydrocarbon receptor (en)
|
http://linked.open.../riv/klicoveSlovo
| |
http://linked.open...odStatuVydavatele
| |
http://linked.open...ontrolniKodProRIV
| |
http://linked.open...i/riv/nazevZdroje
| |
http://linked.open...in/vavai/riv/obor
| |
http://linked.open...ichTvurcuVysledku
| |
http://linked.open...cetTvurcuVysledku
| |
http://linked.open...vavai/riv/projekt
| |
http://linked.open...UplatneniVysledku
| |
http://linked.open...v/svazekPeriodika
| |
http://linked.open...iv/tvurceVysledku
| - Dvořák, Zdeněk
- Pávek, Petr
- Vrzal, Radim
- Stejskalová, Lucie
- Rulcová, Alice
|
http://linked.open...ain/vavai/riv/wos
| |
issn
| |
number of pages
| |
http://bibframe.org/vocab/doi
| - 10.1016/j.toxlet.2013.09.014
|
http://localhost/t...ganizacniJednotka
| |