Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells

Autores
Bussmann, Ursula Agnes; Barañao, Jose Lino Salvador
Año de publicación
2008
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The aryl hydrocarbon receptor (AHR) mediates toxic responses to environmental contaminants and plays pivotal physiological roles in various biological processes as well, particularly in ovarian function. It is well documented that expression and function of the AHR is negatively regulated by transforming growth factor-beta (TGF-beta) in many cell types. In addition, several studies indicate that AHR activity inhibits TGF-beta expression and function in some systems. However, the interplay between these two signals is highly dependent upon the cell type being studied, precluding a generalization about the outcome of such interaction. Therefore, the goal of the present study was to determine the effect of TGF-beta on AHR expression and activation in granulosa cells, an ovarian cell type where the growth factor is mitogenic and AHR activation has been associated with promotion of proliferation as well. In addition, we conducted experiments aimed at evaluating the effect of AHR ligands on TGF-beta action in our system. Results presented herein demonstrate that AHR expression is not regulated by TGF-beta in rat granulosa cells, neither at the mRNA level nor at the protein level. Moreover, we find that the growth factor does not alter the transcriptional function of the AHR. Conversely, we show that activation of AHR by an agonist deregulates TGF-beta function in granulosa cells, inhibiting its transcriptional activity and its mitogenic action. The described one-sided interplay between TGF-beta and AHR signaling pathway may help provide a mechanistic explanation to some of the physiological outcomes of AHR or TGF-beta activation in granulosa cells.
Fil: Bussmann, Ursula Agnes. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Barañao, Jose Lino Salvador. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina
Materia
Aryl Hydrocarbon Receptor
Transforming Growth Factor Beta
Granulosa Cells
Beta Naphthoflavone
Proliferation
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/25464
Acceder
id CONICETDig_50c23da1097bd1c060525b215e34c477
oai_identifier_str oai:ri.conicet.gov.ar:11336/25464
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cellsBussmann, Ursula AgnesBarañao, Jose Lino SalvadorAryl Hydrocarbon ReceptorTransforming Growth Factor BetaGranulosa CellsBeta NaphthoflavoneProliferationhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The aryl hydrocarbon receptor (AHR) mediates toxic responses to environmental contaminants and plays pivotal physiological roles in various biological processes as well, particularly in ovarian function. It is well documented that expression and function of the AHR is negatively regulated by transforming growth factor-beta (TGF-beta) in many cell types. In addition, several studies indicate that AHR activity inhibits TGF-beta expression and function in some systems. However, the interplay between these two signals is highly dependent upon the cell type being studied, precluding a generalization about the outcome of such interaction. Therefore, the goal of the present study was to determine the effect of TGF-beta on AHR expression and activation in granulosa cells, an ovarian cell type where the growth factor is mitogenic and AHR activation has been associated with promotion of proliferation as well. In addition, we conducted experiments aimed at evaluating the effect of AHR ligands on TGF-beta action in our system. Results presented herein demonstrate that AHR expression is not regulated by TGF-beta in rat granulosa cells, neither at the mRNA level nor at the protein level. Moreover, we find that the growth factor does not alter the transcriptional function of the AHR. Conversely, we show that activation of AHR by an agonist deregulates TGF-beta function in granulosa cells, inhibiting its transcriptional activity and its mitogenic action. The described one-sided interplay between TGF-beta and AHR signaling pathway may help provide a mechanistic explanation to some of the physiological outcomes of AHR or TGF-beta activation in granulosa cells.Fil: Bussmann, Ursula Agnes. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Barañao, Jose Lino Salvador. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; ArgentinaElsevier2008-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/25464Bussmann, Ursula Agnes; Barañao, Jose Lino Salvador; Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells; Elsevier; Biochemical Pharmacology; 76; 9; 10-2008; 1165-11740006-29521873-2968CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0006295208005625info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bcp.2008.08.019info:eu-repo/semantics/altIdentifier/pmid/18786509info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:47:12Zoai:ri.conicet.gov.ar:11336/25464instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:47:12.39CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
title Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
spellingShingle Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
Bussmann, Ursula Agnes
Aryl Hydrocarbon Receptor
Transforming Growth Factor Beta
Granulosa Cells
Beta Naphthoflavone
Proliferation
title_short Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
title_full Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
title_fullStr Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
title_full_unstemmed Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
title_sort Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells
dc.creator.none.fl_str_mv Bussmann, Ursula Agnes
Barañao, Jose Lino Salvador
author Bussmann, Ursula Agnes
author_facet Bussmann, Ursula Agnes
Barañao, Jose Lino Salvador
author_role author
author2 Barañao, Jose Lino Salvador
author2_role author
dc.subject.none.fl_str_mv Aryl Hydrocarbon Receptor
Transforming Growth Factor Beta
Granulosa Cells
Beta Naphthoflavone
Proliferation
topic Aryl Hydrocarbon Receptor
Transforming Growth Factor Beta
Granulosa Cells
Beta Naphthoflavone
Proliferation
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The aryl hydrocarbon receptor (AHR) mediates toxic responses to environmental contaminants and plays pivotal physiological roles in various biological processes as well, particularly in ovarian function. It is well documented that expression and function of the AHR is negatively regulated by transforming growth factor-beta (TGF-beta) in many cell types. In addition, several studies indicate that AHR activity inhibits TGF-beta expression and function in some systems. However, the interplay between these two signals is highly dependent upon the cell type being studied, precluding a generalization about the outcome of such interaction. Therefore, the goal of the present study was to determine the effect of TGF-beta on AHR expression and activation in granulosa cells, an ovarian cell type where the growth factor is mitogenic and AHR activation has been associated with promotion of proliferation as well. In addition, we conducted experiments aimed at evaluating the effect of AHR ligands on TGF-beta action in our system. Results presented herein demonstrate that AHR expression is not regulated by TGF-beta in rat granulosa cells, neither at the mRNA level nor at the protein level. Moreover, we find that the growth factor does not alter the transcriptional function of the AHR. Conversely, we show that activation of AHR by an agonist deregulates TGF-beta function in granulosa cells, inhibiting its transcriptional activity and its mitogenic action. The described one-sided interplay between TGF-beta and AHR signaling pathway may help provide a mechanistic explanation to some of the physiological outcomes of AHR or TGF-beta activation in granulosa cells.
Fil: Bussmann, Ursula Agnes. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Barañao, Jose Lino Salvador. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina
description The aryl hydrocarbon receptor (AHR) mediates toxic responses to environmental contaminants and plays pivotal physiological roles in various biological processes as well, particularly in ovarian function. It is well documented that expression and function of the AHR is negatively regulated by transforming growth factor-beta (TGF-beta) in many cell types. In addition, several studies indicate that AHR activity inhibits TGF-beta expression and function in some systems. However, the interplay between these two signals is highly dependent upon the cell type being studied, precluding a generalization about the outcome of such interaction. Therefore, the goal of the present study was to determine the effect of TGF-beta on AHR expression and activation in granulosa cells, an ovarian cell type where the growth factor is mitogenic and AHR activation has been associated with promotion of proliferation as well. In addition, we conducted experiments aimed at evaluating the effect of AHR ligands on TGF-beta action in our system. Results presented herein demonstrate that AHR expression is not regulated by TGF-beta in rat granulosa cells, neither at the mRNA level nor at the protein level. Moreover, we find that the growth factor does not alter the transcriptional function of the AHR. Conversely, we show that activation of AHR by an agonist deregulates TGF-beta function in granulosa cells, inhibiting its transcriptional activity and its mitogenic action. The described one-sided interplay between TGF-beta and AHR signaling pathway may help provide a mechanistic explanation to some of the physiological outcomes of AHR or TGF-beta activation in granulosa cells.
publishDate 2008
dc.date.none.fl_str_mv 2008-10
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/11336/25464
Bussmann, Ursula Agnes; Barañao, Jose Lino Salvador; Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells; Elsevier; Biochemical Pharmacology; 76; 9; 10-2008; 1165-1174
0006-2952
1873-2968
CONICET Digital
CONICET
url http://hdl.handle.net/11336/25464
identifier_str_mv Bussmann, Ursula Agnes; Barañao, Jose Lino Salvador; Interaction between the aryl hydrocarbon receptor and transforming growth factor-beta signaling pathways: evidence of an asymmetrical relationship in rat granulosa cells; Elsevier; Biochemical Pharmacology; 76; 9; 10-2008; 1165-1174
0006-2952
1873-2968
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0006295208005625
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bcp.2008.08.019
info:eu-repo/semantics/altIdentifier/pmid/18786509
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1846782176900677632
score 13.199325

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