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
- Institución
- Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
- OAI Identificador
- paperaa:paper_00063363_v74_n2_p417_Bussmann
Ver los metadatos del registro completo
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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 |
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Biblioteca Digital (UBA-FCEN) |
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Biblioteca Digital (UBA-FCEN) |
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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 |
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ana@bl.fcen.uba.ar |
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