IBYME   02675
INSTITUTO DE BIOLOGIA Y MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
artículos
Título:
Aryl hydrocarbon receptor activation leads to impairment of estrogen-driven chicken vitellogenin promoter activity in LMH cells
Autor/es:
BUSSMANN URSULA ; PEREZ SAEZ JUAN MANUEL; BUSSMANN LEONARDO; BARAÑAO J LINO
Revista:
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY. TOXICOLOGY & PHARMACOLOGY
Editorial:
ELSEVIER SCIENCE INC
Referencias:
Año: 2012 vol. 157 p. 111 - 118
ISSN:
1532-0456
Resumen:
The Aryl Hydrocarbon Receptor (AHR) is a ligand-activated transcription factor that
mediates most of the toxic effects of environmental contaminants. Among the multiple
pleiotropic responses elicited by AHR agonists, the antiestrogenic and endocrine-disrupting
action of the receptor activation is the most studied. It has been demonstrated that some
AHR agonists disrupt estradiol-induced vitellogenin synthesis in the fish liver via a
mechanism that involves crosstalk between the AHR and the Estrogen Receptor (ER).
Chicken hepatocytes have become a model for the study of AHR action in birds and the
induction of the signal and its effect in these cells are well established. However, the impact
of AHR activation on estradiol-regulated responses in the chicken liver remains to be
demonstrated. The aim of the present study was, therefore, to determine the effect of AHR
action on ER-driven transcription in a convenient model of chicken liver cells. For this
purpose, we designed a reporter construct bearing the 5? regulatory region of the chickened a reporter construct bearing the 5? regulatory region of the chicken
vitellogenin II gene and used it to transfect chicken hepatoma LMH cells. We found that â-
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.
and used it to transfect chicken hepatoma LMH cells. We found that â-
naphthoflavone represses ER-driven vitellogenin promoter activity and that this action is
mediated by the AHR. This inhibitory crosstalk between both pathways appears to be
unidirectional, since estradiol did not alter the transcript levels of an AHR target gene.
Besides, and highly relevant, we show that LMH cell line transfected with a reporter
construct bearing the chicken vitellogenin promoter sequence is a useful and convenient
model for the study of AHR-ER interaction in chicken liver-derived cells.