PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress

Autores
Uranga, Romina Maria; Giusto, Norma Maria; Salvador, Gabriela Alejandra
Año de publicación
2011
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
We have previously demonstrated the alteration of cell viability, morphology and lipid peroxidation as well as the activation of PI3K/Akt/GSK3ß pathway in a model of iron-induced neurodegeneration. The exposure of a mouse hippocampal neuronal 2+ cell line (HT22) to different concentrations of Fe (25-200 μM) for 2+ 24 h led us to define a mild oxidative injury status (25-50 μM Fe ). The aim of this work was to investigate the involvement of FoxO transcription factors, known downstream effectors of PI3K, during iron-triggered mild oxidative stress. Under this experimental condition, reactive oxygen species measured by fluorescence microscopy increased with small changes in cell viability, and SOD1 levels decreased whereas catalase levels showed no changes with respect to controls. The localization of phosphorylated and non-phosphorylated FoxO3a was studied in nuclear and cytosolic fractions. Levels of phospho-FoxO3a (the inactive form) increased in the cytosolic fraction of cells treated with iron in a PI3K- dependent manner. Consistent with this, total FoxO3a content decreased in the nuclear fraction. FoxO1 phosphorylation also increased in the cytosolic fraction. Our results show that iron- induced neurotoxicity activates PI3K/Akt/GSK3ß promoting FoxO3a/FoxO1 phosphorylation, their inactivation and their cytosolic localization under mild oxidative injury in hippocampal neurons
Fil: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Giusto, Norma Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Potrero de los Funes
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Materia
AKT
PI3K
FOXO TRANSCRIPTION FACTORS
OXIDATIVE STRESS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/246945
Acceder
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network_name_str CONICET Digital (CONICET)
spelling PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stressUranga, Romina MariaGiusto, Norma MariaSalvador, Gabriela AlejandraAKTPI3KFOXO TRANSCRIPTION FACTORSOXIDATIVE STRESShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1We have previously demonstrated the alteration of cell viability, morphology and lipid peroxidation as well as the activation of PI3K/Akt/GSK3ß pathway in a model of iron-induced neurodegeneration. The exposure of a mouse hippocampal neuronal 2+ cell line (HT22) to different concentrations of Fe (25-200 μM) for 2+ 24 h led us to define a mild oxidative injury status (25-50 μM Fe ). The aim of this work was to investigate the involvement of FoxO transcription factors, known downstream effectors of PI3K, during iron-triggered mild oxidative stress. Under this experimental condition, reactive oxygen species measured by fluorescence microscopy increased with small changes in cell viability, and SOD1 levels decreased whereas catalase levels showed no changes with respect to controls. The localization of phosphorylated and non-phosphorylated FoxO3a was studied in nuclear and cytosolic fractions. Levels of phospho-FoxO3a (the inactive form) increased in the cytosolic fraction of cells treated with iron in a PI3K- dependent manner. Consistent with this, total FoxO3a content decreased in the nuclear fraction. FoxO1 phosphorylation also increased in the cytosolic fraction. Our results show that iron- induced neurotoxicity activates PI3K/Akt/GSK3ß promoting FoxO3a/FoxO1 phosphorylation, their inactivation and their cytosolic localization under mild oxidative injury in hippocampal neuronsFil: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Giusto, Norma Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaXLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología MolecularPotrero de los FunesArgentinaSociedad Argentina de Investigación en Bioquímica y Biología MolecularInstituto de Histología y Embriología “Dr. Mario H. Burgos”2011info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/246945PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Potrero de los Funes; Argentina; 2011; 130-1300327-95451667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://saib.org.ar/publicaciones/Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:04:17Zoai:ri.conicet.gov.ar:11336/246945instacron: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:34982025-10-15 15:04:17.647CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
title PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
spellingShingle PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
Uranga, Romina Maria
AKT
PI3K
FOXO TRANSCRIPTION FACTORS
OXIDATIVE STRESS
title_short PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
title_full PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
title_fullStr PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
title_full_unstemmed PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
title_sort PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress
dc.creator.none.fl_str_mv Uranga, Romina Maria
Giusto, Norma Maria
Salvador, Gabriela Alejandra
author Uranga, Romina Maria
author_facet Uranga, Romina Maria
Giusto, Norma Maria
Salvador, Gabriela Alejandra
author_role author
author2 Giusto, Norma Maria
Salvador, Gabriela Alejandra
author2_role author
author
dc.subject.none.fl_str_mv AKT
PI3K
FOXO TRANSCRIPTION FACTORS
OXIDATIVE STRESS
topic AKT
PI3K
FOXO TRANSCRIPTION FACTORS
OXIDATIVE STRESS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv We have previously demonstrated the alteration of cell viability, morphology and lipid peroxidation as well as the activation of PI3K/Akt/GSK3ß pathway in a model of iron-induced neurodegeneration. The exposure of a mouse hippocampal neuronal 2+ cell line (HT22) to different concentrations of Fe (25-200 μM) for 2+ 24 h led us to define a mild oxidative injury status (25-50 μM Fe ). The aim of this work was to investigate the involvement of FoxO transcription factors, known downstream effectors of PI3K, during iron-triggered mild oxidative stress. Under this experimental condition, reactive oxygen species measured by fluorescence microscopy increased with small changes in cell viability, and SOD1 levels decreased whereas catalase levels showed no changes with respect to controls. The localization of phosphorylated and non-phosphorylated FoxO3a was studied in nuclear and cytosolic fractions. Levels of phospho-FoxO3a (the inactive form) increased in the cytosolic fraction of cells treated with iron in a PI3K- dependent manner. Consistent with this, total FoxO3a content decreased in the nuclear fraction. FoxO1 phosphorylation also increased in the cytosolic fraction. Our results show that iron- induced neurotoxicity activates PI3K/Akt/GSK3ß promoting FoxO3a/FoxO1 phosphorylation, their inactivation and their cytosolic localization under mild oxidative injury in hippocampal neurons
Fil: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Giusto, Norma Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Potrero de los Funes
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
description We have previously demonstrated the alteration of cell viability, morphology and lipid peroxidation as well as the activation of PI3K/Akt/GSK3ß pathway in a model of iron-induced neurodegeneration. The exposure of a mouse hippocampal neuronal 2+ cell line (HT22) to different concentrations of Fe (25-200 μM) for 2+ 24 h led us to define a mild oxidative injury status (25-50 μM Fe ). The aim of this work was to investigate the involvement of FoxO transcription factors, known downstream effectors of PI3K, during iron-triggered mild oxidative stress. Under this experimental condition, reactive oxygen species measured by fluorescence microscopy increased with small changes in cell viability, and SOD1 levels decreased whereas catalase levels showed no changes with respect to controls. The localization of phosphorylated and non-phosphorylated FoxO3a was studied in nuclear and cytosolic fractions. Levels of phospho-FoxO3a (the inactive form) increased in the cytosolic fraction of cells treated with iron in a PI3K- dependent manner. Consistent with this, total FoxO3a content decreased in the nuclear fraction. FoxO1 phosphorylation also increased in the cytosolic fraction. Our results show that iron- induced neurotoxicity activates PI3K/Akt/GSK3ß promoting FoxO3a/FoxO1 phosphorylation, their inactivation and their cytosolic localization under mild oxidative injury in hippocampal neurons
publishDate 2011
dc.date.none.fl_str_mv 2011
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Congreso
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/246945
PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Potrero de los Funes; Argentina; 2011; 130-130
0327-9545
1667-5746
CONICET Digital
CONICET
url http://hdl.handle.net/11336/246945
identifier_str_mv PI3K-dependent inactivation of FoxO transcription factors in a hippocampal model of oxidative stress; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Potrero de los Funes; Argentina; 2011; 130-130
0327-9545
1667-5746
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://saib.org.ar/publicaciones/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Nacional
dc.publisher.none.fl_str_mv Instituto de Histología y Embriología “Dr. Mario H. Burgos”
publisher.none.fl_str_mv Instituto de Histología y Embriología “Dr. Mario H. Burgos”
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
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score 13.22299

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