The levels of RAC3 expression are up regulated by TNF in the inflammatory response

Autores
Alvarado, Cecilia Viviana; Rubio, Maria Fernanda; Fernández Larrosa, Pablo Nicolás; Panelo, Laura Carolina; Azurmendi, Pablo Javier; Ruiz Grecco, Marina; Martínez Noël, Giselle María Astrid; Costas, Monica Alejandra
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
RAC3 is a coactivator of glucocorticoid receptor and nuclear factor-κB (NF-κB) that is usually over-expressed in tumors and which also has important functions in the immune system. We investigated the role of the inflammatory response in the control of RAC3 expression levels in vivo and in vitro. We found that inflammation regulates RAC3 levels. In mice, sub-lethal doses of lipopolysaccharide induce the increase of RAC3 in spleen and the administration of the synthetic anti-inflammatory glucocorticoid dexamethasone has a similar effect. However, the simultaneous treatment with both stimuli is mutually antagonistic. In vitro stimulation of the HEK293 cell line with tumor necrosis factor (TNF), one of the cytokines induced by lipopolysaccharide, also increases the levels of RAC3 mRNA and protein, which correlates with an enhanced transcription dependent on the RAC3 gene promoter. We found that binding of the transcription factor NF-κB to the RAC3 gene promoter could be responsible for these effects. Although glucocorticoid alone has the same effect that TNF, no synergism or antagonism was observed in vitro by simultaneous stimulation. Our results suggest that increase of RAC3 during inflammation or an anti-inflammatory response could be a molecular mechanism involved in the control of sensitivity to both stimuli in order to maintain the normal healthy course of the immune response.
Fil: Alvarado, Cecilia Viviana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Rubio, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Fernández Larrosa, Pablo Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Azurmendi, Pablo Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Ruiz Grecco, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Martínez Noël, Giselle María Astrid. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Materia
Rac·
Glucocorticoid
Tnf
Nf-Kb
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:11336/29431
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The levels of RAC3 expression are up regulated by TNF in the inflammatory responseAlvarado, Cecilia VivianaRubio, Maria FernandaFernández Larrosa, Pablo NicolásPanelo, Laura CarolinaAzurmendi, Pablo JavierRuiz Grecco, MarinaMartínez Noël, Giselle María AstridCostas, Monica AlejandraRac·GlucocorticoidTnfNf-Kbhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3RAC3 is a coactivator of glucocorticoid receptor and nuclear factor-κB (NF-κB) that is usually over-expressed in tumors and which also has important functions in the immune system. We investigated the role of the inflammatory response in the control of RAC3 expression levels in vivo and in vitro. We found that inflammation regulates RAC3 levels. In mice, sub-lethal doses of lipopolysaccharide induce the increase of RAC3 in spleen and the administration of the synthetic anti-inflammatory glucocorticoid dexamethasone has a similar effect. However, the simultaneous treatment with both stimuli is mutually antagonistic. In vitro stimulation of the HEK293 cell line with tumor necrosis factor (TNF), one of the cytokines induced by lipopolysaccharide, also increases the levels of RAC3 mRNA and protein, which correlates with an enhanced transcription dependent on the RAC3 gene promoter. We found that binding of the transcription factor NF-κB to the RAC3 gene promoter could be responsible for these effects. Although glucocorticoid alone has the same effect that TNF, no synergism or antagonism was observed in vitro by simultaneous stimulation. Our results suggest that increase of RAC3 during inflammation or an anti-inflammatory response could be a molecular mechanism involved in the control of sensitivity to both stimuli in order to maintain the normal healthy course of the immune response.Fil: Alvarado, Cecilia Viviana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Rubio, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Fernández Larrosa, Pablo Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Azurmendi, Pablo Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Ruiz Grecco, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Martínez Noël, Giselle María Astrid. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaWiley2014-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/29431Alvarado, Cecilia Viviana; Rubio, Maria Fernanda; Fernández Larrosa, Pablo Nicolás; Panelo, Laura Carolina; Azurmendi, Pablo Javier; et al.; The levels of RAC3 expression are up regulated by TNF in the inflammatory response; Wiley; Febs Open Bio; 4; 1; 1-2014; 450-4572211-5463CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.fob.2014.04.009info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1016/j.fob.2014.04.009/abstractinfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050193/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:35:36Zoai:ri.conicet.gov.ar:11336/29431instacron: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:34982025-09-29 09:35:37.151CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The levels of RAC3 expression are up regulated by TNF in the inflammatory response
title The levels of RAC3 expression are up regulated by TNF in the inflammatory response
spellingShingle The levels of RAC3 expression are up regulated by TNF in the inflammatory response
Alvarado, Cecilia Viviana
Rac·
Glucocorticoid
Tnf
Nf-Kb
title_short The levels of RAC3 expression are up regulated by TNF in the inflammatory response
title_full The levels of RAC3 expression are up regulated by TNF in the inflammatory response
title_fullStr The levels of RAC3 expression are up regulated by TNF in the inflammatory response
title_full_unstemmed The levels of RAC3 expression are up regulated by TNF in the inflammatory response
title_sort The levels of RAC3 expression are up regulated by TNF in the inflammatory response
dc.creator.none.fl_str_mv Alvarado, Cecilia Viviana
Rubio, Maria Fernanda
Fernández Larrosa, Pablo Nicolás
Panelo, Laura Carolina
Azurmendi, Pablo Javier
Ruiz Grecco, Marina
Martínez Noël, Giselle María Astrid
Costas, Monica Alejandra
author Alvarado, Cecilia Viviana
author_facet Alvarado, Cecilia Viviana
Rubio, Maria Fernanda
Fernández Larrosa, Pablo Nicolás
Panelo, Laura Carolina
Azurmendi, Pablo Javier
Ruiz Grecco, Marina
Martínez Noël, Giselle María Astrid
Costas, Monica Alejandra
author_role author
author2 Rubio, Maria Fernanda
Fernández Larrosa, Pablo Nicolás
Panelo, Laura Carolina
Azurmendi, Pablo Javier
Ruiz Grecco, Marina
Martínez Noël, Giselle María Astrid
Costas, Monica Alejandra
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Rac·
Glucocorticoid
Tnf
Nf-Kb
topic Rac·
Glucocorticoid
Tnf
Nf-Kb
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv RAC3 is a coactivator of glucocorticoid receptor and nuclear factor-κB (NF-κB) that is usually over-expressed in tumors and which also has important functions in the immune system. We investigated the role of the inflammatory response in the control of RAC3 expression levels in vivo and in vitro. We found that inflammation regulates RAC3 levels. In mice, sub-lethal doses of lipopolysaccharide induce the increase of RAC3 in spleen and the administration of the synthetic anti-inflammatory glucocorticoid dexamethasone has a similar effect. However, the simultaneous treatment with both stimuli is mutually antagonistic. In vitro stimulation of the HEK293 cell line with tumor necrosis factor (TNF), one of the cytokines induced by lipopolysaccharide, also increases the levels of RAC3 mRNA and protein, which correlates with an enhanced transcription dependent on the RAC3 gene promoter. We found that binding of the transcription factor NF-κB to the RAC3 gene promoter could be responsible for these effects. Although glucocorticoid alone has the same effect that TNF, no synergism or antagonism was observed in vitro by simultaneous stimulation. Our results suggest that increase of RAC3 during inflammation or an anti-inflammatory response could be a molecular mechanism involved in the control of sensitivity to both stimuli in order to maintain the normal healthy course of the immune response.
Fil: Alvarado, Cecilia Viviana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Rubio, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Fernández Larrosa, Pablo Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Azurmendi, Pablo Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Ruiz Grecco, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Martínez Noël, Giselle María Astrid. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
description RAC3 is a coactivator of glucocorticoid receptor and nuclear factor-κB (NF-κB) that is usually over-expressed in tumors and which also has important functions in the immune system. We investigated the role of the inflammatory response in the control of RAC3 expression levels in vivo and in vitro. We found that inflammation regulates RAC3 levels. In mice, sub-lethal doses of lipopolysaccharide induce the increase of RAC3 in spleen and the administration of the synthetic anti-inflammatory glucocorticoid dexamethasone has a similar effect. However, the simultaneous treatment with both stimuli is mutually antagonistic. In vitro stimulation of the HEK293 cell line with tumor necrosis factor (TNF), one of the cytokines induced by lipopolysaccharide, also increases the levels of RAC3 mRNA and protein, which correlates with an enhanced transcription dependent on the RAC3 gene promoter. We found that binding of the transcription factor NF-κB to the RAC3 gene promoter could be responsible for these effects. Although glucocorticoid alone has the same effect that TNF, no synergism or antagonism was observed in vitro by simultaneous stimulation. Our results suggest that increase of RAC3 during inflammation or an anti-inflammatory response could be a molecular mechanism involved in the control of sensitivity to both stimuli in order to maintain the normal healthy course of the immune response.
publishDate 2014
dc.date.none.fl_str_mv 2014-01
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/11336/29431
Alvarado, Cecilia Viviana; Rubio, Maria Fernanda; Fernández Larrosa, Pablo Nicolás; Panelo, Laura Carolina; Azurmendi, Pablo Javier; et al.; The levels of RAC3 expression are up regulated by TNF in the inflammatory response; Wiley; Febs Open Bio; 4; 1; 1-2014; 450-457
2211-5463
CONICET Digital
CONICET
url http://hdl.handle.net/11336/29431
identifier_str_mv Alvarado, Cecilia Viviana; Rubio, Maria Fernanda; Fernández Larrosa, Pablo Nicolás; Panelo, Laura Carolina; Azurmendi, Pablo Javier; et al.; The levels of RAC3 expression are up regulated by TNF in the inflammatory response; Wiley; Febs Open Bio; 4; 1; 1-2014; 450-457
2211-5463
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.fob.2014.04.009
info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1016/j.fob.2014.04.009/abstract
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050193/
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
application/pdf
application/pdf
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application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
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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
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