An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors

Autores
Bussmann, U.A.; Bussmann, L.E.; Barañao, J.L.
Año de publicación
2006
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that, besides mediating toxic responses, may have a central role in ovarian physiology. Studying the actions of AHR ligands on granulosa cells function, we have found that beta-naphthoflavone amplifies the comitogenic actions of FSH and 17beta-estradiol in a dose-dependent manner. This amplification was even greater in cells that overexpress the AHR and was reversed by cotreatment with the AHR antagonist alpha-naphthoflavone, suggesting that this effect is mediated by the AHR. The estrogen receptor is likewise implicated in this phenomenon, because a pure antiestrogen abolished the described synergism. However, the more traditional inhibitory AHR-estrogen receptor interaction was observed on the estrogen response element-driven transcriptional activity. On the other hand, alpha-naphthoflavone inhibited dose-dependently the mitogenic actions of FSH and 17beta-estradiol. Beta-naphthoflavone induced the expression of Cyp1a1 and Cyp1b1 transcripts, two well-characterized AHR-inducible genes that code for hydroxylases that metabolize estradiol to catecholestrogens. Nevertheless, the positive effect of beta-naphthoflavone on proliferation was not caused by increased metabolism of estradiol to catecholestrogens, because these compounds inhibited the hormonally stimulated DNA synthesis. This latter inhibition exerted by catecholestrogens suggests that these hydroxylases would play a regulatory point in granulosa cell proliferation. Our study indicates that AHR ligands modulate the proliferation of rat granulosa cells, and demonstrates for the first time that an agonist of this receptor is able to amplify the comitogenic action of classical hormones through a mechanism that might implicate a positive cross-talk between the AHR and the estrogen receptor pathways. © 2006 by the Society for the Study of Reproduction, Inc.
Fil:Bussmann, U.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Barañao, J.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fuente
Biol. Reprod. 2006;74(2):417-426
Materia
Estradiol
Estradiol receptor
Granulosa cells
Ovary
Toxicology
alpha naphthoflavone
aromatic hydrocarbon receptor
beta naphthoflavone
catechol estrogen
cytochrome P450 1A1
cytochrome P450 1B1
estradiol
estrogen receptor
follitropin
oxygenase
animal cell
animal tissue
article
cell proliferation
controlled study
DNA synthesis
dose response
estrogen metabolism
female
genetic transcription
granulosa cell
mitogenesis
nonhuman
ovary
priority journal
rat
signal transduction
Animals
Aryl Hydrocarbon Hydroxylases
Benzoflavones
beta-Naphthoflavone
Cells, Cultured
Cytochrome P-450 CYP1A1
DNA
Drug Synergism
Estradiol
Estrogens, Catechol
Female
Follicle Stimulating Hormone
Granulosa Cells
Mitogens
Rats
Rats, Sprague-Dawley
Receptors, Aryl Hydrocarbon
Receptors, Estrogen
RNA, Messenger
Trans-Activation (Genetics)
Animalia
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/2.5/ar
Repositorio
Biblioteca Digital (UBA-FCEN)
Institución
Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
OAI Identificador
paperaa:paper_00063363_v74_n2_p417_Bussmann

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oai_identifier_str paperaa:paper_00063363_v74_n2_p417_Bussmann
network_acronym_str BDUBAFCEN
repository_id_str 1896
network_name_str Biblioteca Digital (UBA-FCEN)
spelling An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptorsBussmann, U.A.Bussmann, L.E.Barañao, J.L.EstradiolEstradiol receptorGranulosa cellsOvaryToxicologyalpha naphthoflavonearomatic hydrocarbon receptorbeta naphthoflavonecatechol estrogencytochrome P450 1A1cytochrome P450 1B1estradiolestrogen receptorfollitropinoxygenaseanimal cellanimal tissuearticlecell proliferationcontrolled studyDNA synthesisdose responseestrogen metabolismfemalegenetic transcriptiongranulosa cellmitogenesisnonhumanovarypriority journalratsignal transductionAnimalsAryl Hydrocarbon HydroxylasesBenzoflavonesbeta-NaphthoflavoneCells, CulturedCytochrome P-450 CYP1A1DNADrug SynergismEstradiolEstrogens, CatecholFemaleFollicle Stimulating HormoneGranulosa CellsMitogensRatsRats, Sprague-DawleyReceptors, Aryl HydrocarbonReceptors, EstrogenRNA, MessengerTrans-Activation (Genetics)AnimaliaThe aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that, besides mediating toxic responses, may have a central role in ovarian physiology. Studying the actions of AHR ligands on granulosa cells function, we have found that beta-naphthoflavone amplifies the comitogenic actions of FSH and 17beta-estradiol in a dose-dependent manner. This amplification was even greater in cells that overexpress the AHR and was reversed by cotreatment with the AHR antagonist alpha-naphthoflavone, suggesting that this effect is mediated by the AHR. The estrogen receptor is likewise implicated in this phenomenon, because a pure antiestrogen abolished the described synergism. However, the more traditional inhibitory AHR-estrogen receptor interaction was observed on the estrogen response element-driven transcriptional activity. On the other hand, alpha-naphthoflavone inhibited dose-dependently the mitogenic actions of FSH and 17beta-estradiol. Beta-naphthoflavone induced the expression of Cyp1a1 and Cyp1b1 transcripts, two well-characterized AHR-inducible genes that code for hydroxylases that metabolize estradiol to catecholestrogens. Nevertheless, the positive effect of beta-naphthoflavone on proliferation was not caused by increased metabolism of estradiol to catecholestrogens, because these compounds inhibited the hormonally stimulated DNA synthesis. This latter inhibition exerted by catecholestrogens suggests that these hydroxylases would play a regulatory point in granulosa cell proliferation. Our study indicates that AHR ligands modulate the proliferation of rat granulosa cells, and demonstrates for the first time that an agonist of this receptor is able to amplify the comitogenic action of classical hormones through a mechanism that might implicate a positive cross-talk between the AHR and the estrogen receptor pathways. © 2006 by the Society for the Study of Reproduction, Inc.Fil:Bussmann, U.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.Fil:Barañao, J.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.2006info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://hdl.handle.net/20.500.12110/paper_00063363_v74_n2_p417_BussmannBiol. Reprod. 2006;74(2):417-426reponame:Biblioteca Digital (UBA-FCEN)instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesinstacron:UBA-FCENenginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/2.5/ar2025-09-29T13:42:52Zpaperaa:paper_00063363_v74_n2_p417_BussmannInstitucionalhttps://digital.bl.fcen.uba.ar/Universidad públicaNo correspondehttps://digital.bl.fcen.uba.ar/cgi-bin/oaiserver.cgiana@bl.fcen.uba.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:18962025-09-29 13:42:53.354Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesfalse
dc.title.none.fl_str_mv An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
title An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
spellingShingle An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
Bussmann, U.A.
Estradiol
Estradiol receptor
Granulosa cells
Ovary
Toxicology
alpha naphthoflavone
aromatic hydrocarbon receptor
beta naphthoflavone
catechol estrogen
cytochrome P450 1A1
cytochrome P450 1B1
estradiol
estrogen receptor
follitropin
oxygenase
animal cell
animal tissue
article
cell proliferation
controlled study
DNA synthesis
dose response
estrogen metabolism
female
genetic transcription
granulosa cell
mitogenesis
nonhuman
ovary
priority journal
rat
signal transduction
Animals
Aryl Hydrocarbon Hydroxylases
Benzoflavones
beta-Naphthoflavone
Cells, Cultured
Cytochrome P-450 CYP1A1
DNA
Drug Synergism
Estradiol
Estrogens, Catechol
Female
Follicle Stimulating Hormone
Granulosa Cells
Mitogens
Rats
Rats, Sprague-Dawley
Receptors, Aryl Hydrocarbon
Receptors, Estrogen
RNA, Messenger
Trans-Activation (Genetics)
Animalia
title_short An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
title_full An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
title_fullStr An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
title_full_unstemmed An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
title_sort An aryl hydrocarbon receptor agonist amplifies the mitogenic actions of estradiol in granulosa cells: Evidence of involvement of the cognate receptors
dc.creator.none.fl_str_mv Bussmann, U.A.
Bussmann, L.E.
Barañao, J.L.
author Bussmann, U.A.
author_facet Bussmann, U.A.
Bussmann, L.E.
Barañao, J.L.
author_role author
author2 Bussmann, L.E.
Barañao, J.L.
author2_role author
author
dc.subject.none.fl_str_mv Estradiol
Estradiol receptor
Granulosa cells
Ovary
Toxicology
alpha naphthoflavone
aromatic hydrocarbon receptor
beta naphthoflavone
catechol estrogen
cytochrome P450 1A1
cytochrome P450 1B1
estradiol
estrogen receptor
follitropin
oxygenase
animal cell
animal tissue
article
cell proliferation
controlled study
DNA synthesis
dose response
estrogen metabolism
female
genetic transcription
granulosa cell
mitogenesis
nonhuman
ovary
priority journal
rat
signal transduction
Animals
Aryl Hydrocarbon Hydroxylases
Benzoflavones
beta-Naphthoflavone
Cells, Cultured
Cytochrome P-450 CYP1A1
DNA
Drug Synergism
Estradiol
Estrogens, Catechol
Female
Follicle Stimulating Hormone
Granulosa Cells
Mitogens
Rats
Rats, Sprague-Dawley
Receptors, Aryl Hydrocarbon
Receptors, Estrogen
RNA, Messenger
Trans-Activation (Genetics)
Animalia
topic Estradiol
Estradiol receptor
Granulosa cells
Ovary
Toxicology
alpha naphthoflavone
aromatic hydrocarbon receptor
beta naphthoflavone
catechol estrogen
cytochrome P450 1A1
cytochrome P450 1B1
estradiol
estrogen receptor
follitropin
oxygenase
animal cell
animal tissue
article
cell proliferation
controlled study
DNA synthesis
dose response
estrogen metabolism
female
genetic transcription
granulosa cell
mitogenesis
nonhuman
ovary
priority journal
rat
signal transduction
Animals
Aryl Hydrocarbon Hydroxylases
Benzoflavones
beta-Naphthoflavone
Cells, Cultured
Cytochrome P-450 CYP1A1
DNA
Drug Synergism
Estradiol
Estrogens, Catechol
Female
Follicle Stimulating Hormone
Granulosa Cells
Mitogens
Rats
Rats, Sprague-Dawley
Receptors, Aryl Hydrocarbon
Receptors, Estrogen
RNA, Messenger
Trans-Activation (Genetics)
Animalia
dc.description.none.fl_txt_mv The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that, besides mediating toxic responses, may have a central role in ovarian physiology. Studying the actions of AHR ligands on granulosa cells function, we have found that beta-naphthoflavone amplifies the comitogenic actions of FSH and 17beta-estradiol in a dose-dependent manner. This amplification was even greater in cells that overexpress the AHR and was reversed by cotreatment with the AHR antagonist alpha-naphthoflavone, suggesting that this effect is mediated by the AHR. The estrogen receptor is likewise implicated in this phenomenon, because a pure antiestrogen abolished the described synergism. However, the more traditional inhibitory AHR-estrogen receptor interaction was observed on the estrogen response element-driven transcriptional activity. On the other hand, alpha-naphthoflavone inhibited dose-dependently the mitogenic actions of FSH and 17beta-estradiol. Beta-naphthoflavone induced the expression of Cyp1a1 and Cyp1b1 transcripts, two well-characterized AHR-inducible genes that code for hydroxylases that metabolize estradiol to catecholestrogens. Nevertheless, the positive effect of beta-naphthoflavone on proliferation was not caused by increased metabolism of estradiol to catecholestrogens, because these compounds inhibited the hormonally stimulated DNA synthesis. This latter inhibition exerted by catecholestrogens suggests that these hydroxylases would play a regulatory point in granulosa cell proliferation. Our study indicates that AHR ligands modulate the proliferation of rat granulosa cells, and demonstrates for the first time that an agonist of this receptor is able to amplify the comitogenic action of classical hormones through a mechanism that might implicate a positive cross-talk between the AHR and the estrogen receptor pathways. © 2006 by the Society for the Study of Reproduction, Inc.
Fil:Bussmann, U.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Barañao, J.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
description The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that, besides mediating toxic responses, may have a central role in ovarian physiology. Studying the actions of AHR ligands on granulosa cells function, we have found that beta-naphthoflavone amplifies the comitogenic actions of FSH and 17beta-estradiol in a dose-dependent manner. This amplification was even greater in cells that overexpress the AHR and was reversed by cotreatment with the AHR antagonist alpha-naphthoflavone, suggesting that this effect is mediated by the AHR. The estrogen receptor is likewise implicated in this phenomenon, because a pure antiestrogen abolished the described synergism. However, the more traditional inhibitory AHR-estrogen receptor interaction was observed on the estrogen response element-driven transcriptional activity. On the other hand, alpha-naphthoflavone inhibited dose-dependently the mitogenic actions of FSH and 17beta-estradiol. Beta-naphthoflavone induced the expression of Cyp1a1 and Cyp1b1 transcripts, two well-characterized AHR-inducible genes that code for hydroxylases that metabolize estradiol to catecholestrogens. Nevertheless, the positive effect of beta-naphthoflavone on proliferation was not caused by increased metabolism of estradiol to catecholestrogens, because these compounds inhibited the hormonally stimulated DNA synthesis. This latter inhibition exerted by catecholestrogens suggests that these hydroxylases would play a regulatory point in granulosa cell proliferation. Our study indicates that AHR ligands modulate the proliferation of rat granulosa cells, and demonstrates for the first time that an agonist of this receptor is able to amplify the comitogenic action of classical hormones through a mechanism that might implicate a positive cross-talk between the AHR and the estrogen receptor pathways. © 2006 by the Society for the Study of Reproduction, Inc.
publishDate 2006
dc.date.none.fl_str_mv 2006
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.12110/paper_00063363_v74_n2_p417_Bussmann
url http://hdl.handle.net/20.500.12110/paper_00063363_v74_n2_p417_Bussmann
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/2.5/ar
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/2.5/ar
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv Biol. Reprod. 2006;74(2):417-426
reponame:Biblioteca Digital (UBA-FCEN)
instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron:UBA-FCEN
reponame_str Biblioteca Digital (UBA-FCEN)
collection Biblioteca Digital (UBA-FCEN)
instname_str Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron_str UBA-FCEN
institution UBA-FCEN
repository.name.fl_str_mv Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
repository.mail.fl_str_mv ana@bl.fcen.uba.ar
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