Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons

Autores
Uranga, Romina Maria; Rodriguez Diez, Guadalupe; Giusto, Norma Maria; Salvador, Gabriela Alejandra
Año de publicación
2010
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Akt and glycogen synthase kinase 3â (GSK3â) are key components of signaling pathways involved in synaptic plasticity and neuronal survival. The specific aims of this work were: i) to characterize an iron-induced neurodegeneration model and ii) to study the participation of Akt and GSK3â in the signaling events triggered during neuronal oxidative injury. For this purpose, a cell line of 2+ murine hippocampal neurons, HT22, was exposed to increasing Fe concentrations (25, 50, 100 and 200 ìM) for 24 h. Cell viability, morphology and lipid peroxidation were evaluated for determining the extent of neuronal injury. Cell viability, measured as MTT reduction, was significantly reduced in the presence of 50, 100 and 2+ 200 ìM Fe . HT22 cell morphology, evaluated by phase-contrast microscopy, showed evident morphological alterations including rounded cell body with a decreased number of cell projections. The decrease in MTT reduction strongly correlated with the changes in cellular morphology. Based on these data we defined that 24-h exposure to iron (25 and 50 ìM) caused a mild oxidative injury. Under these experimental conditions both Akt and GSK3â phosphorylation were increased. We conclude that iron-induced neurotoxicity activates Akt promoting GSK3â inhibition 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: Rodriguez Diez, Guadalupe. 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
XLVI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Puerto Madryn
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Materia
ESTRÉS OXIDATIVO
SEÑALIZACIÓN
NEUROTOXICIDAD
HIPOCAMPO
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:11336/223463
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/223463
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neuronsUranga, Romina MariaRodriguez Diez, GuadalupeGiusto, Norma MariaSalvador, Gabriela AlejandraESTRÉS OXIDATIVOSEÑALIZACIÓNNEUROTOXICIDADHIPOCAMPOhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Akt and glycogen synthase kinase 3â (GSK3â) are key components of signaling pathways involved in synaptic plasticity and neuronal survival. The specific aims of this work were: i) to characterize an iron-induced neurodegeneration model and ii) to study the participation of Akt and GSK3â in the signaling events triggered during neuronal oxidative injury. For this purpose, a cell line of 2+ murine hippocampal neurons, HT22, was exposed to increasing Fe concentrations (25, 50, 100 and 200 ìM) for 24 h. Cell viability, morphology and lipid peroxidation were evaluated for determining the extent of neuronal injury. Cell viability, measured as MTT reduction, was significantly reduced in the presence of 50, 100 and 2+ 200 ìM Fe . HT22 cell morphology, evaluated by phase-contrast microscopy, showed evident morphological alterations including rounded cell body with a decreased number of cell projections. The decrease in MTT reduction strongly correlated with the changes in cellular morphology. Based on these data we defined that 24-h exposure to iron (25 and 50 ìM) caused a mild oxidative injury. Under these experimental conditions both Akt and GSK3â phosphorylation were increased. We conclude that iron-induced neurotoxicity activates Akt promoting GSK3â inhibition 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; ArgentinaFil: Rodriguez Diez, Guadalupe. 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; ArgentinaXLVI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología MolecularPuerto MadrynArgentinaSociedad Argentina de Investigación en Bioquímica y Biología MolecularBiocell2010info: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/11336/223463Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons; XLVI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Puerto Madryn; Argentina; 2010; 74-740327-95451667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://saib.org.ar/archivos/biocell-34.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:51:16Zoai:ri.conicet.gov.ar:11336/223463instacron: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:34982025-09-03 09:51:16.903CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
title Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
spellingShingle Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
Uranga, Romina Maria
ESTRÉS OXIDATIVO
SEÑALIZACIÓN
NEUROTOXICIDAD
HIPOCAMPO
title_short Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
title_full Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
title_fullStr Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
title_full_unstemmed Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
title_sort Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons
dc.creator.none.fl_str_mv Uranga, Romina Maria
Rodriguez Diez, Guadalupe
Giusto, Norma Maria
Salvador, Gabriela Alejandra
author Uranga, Romina Maria
author_facet Uranga, Romina Maria
Rodriguez Diez, Guadalupe
Giusto, Norma Maria
Salvador, Gabriela Alejandra
author_role author
author2 Rodriguez Diez, Guadalupe
Giusto, Norma Maria
Salvador, Gabriela Alejandra
author2_role author
author
author
dc.subject.none.fl_str_mv ESTRÉS OXIDATIVO
SEÑALIZACIÓN
NEUROTOXICIDAD
HIPOCAMPO
topic ESTRÉS OXIDATIVO
SEÑALIZACIÓN
NEUROTOXICIDAD
HIPOCAMPO
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Akt and glycogen synthase kinase 3â (GSK3â) are key components of signaling pathways involved in synaptic plasticity and neuronal survival. The specific aims of this work were: i) to characterize an iron-induced neurodegeneration model and ii) to study the participation of Akt and GSK3â in the signaling events triggered during neuronal oxidative injury. For this purpose, a cell line of 2+ murine hippocampal neurons, HT22, was exposed to increasing Fe concentrations (25, 50, 100 and 200 ìM) for 24 h. Cell viability, morphology and lipid peroxidation were evaluated for determining the extent of neuronal injury. Cell viability, measured as MTT reduction, was significantly reduced in the presence of 50, 100 and 2+ 200 ìM Fe . HT22 cell morphology, evaluated by phase-contrast microscopy, showed evident morphological alterations including rounded cell body with a decreased number of cell projections. The decrease in MTT reduction strongly correlated with the changes in cellular morphology. Based on these data we defined that 24-h exposure to iron (25 and 50 ìM) caused a mild oxidative injury. Under these experimental conditions both Akt and GSK3â phosphorylation were increased. We conclude that iron-induced neurotoxicity activates Akt promoting GSK3â inhibition 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: Rodriguez Diez, Guadalupe. 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
XLVI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Puerto Madryn
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
description Akt and glycogen synthase kinase 3â (GSK3â) are key components of signaling pathways involved in synaptic plasticity and neuronal survival. The specific aims of this work were: i) to characterize an iron-induced neurodegeneration model and ii) to study the participation of Akt and GSK3â in the signaling events triggered during neuronal oxidative injury. For this purpose, a cell line of 2+ murine hippocampal neurons, HT22, was exposed to increasing Fe concentrations (25, 50, 100 and 200 ìM) for 24 h. Cell viability, morphology and lipid peroxidation were evaluated for determining the extent of neuronal injury. Cell viability, measured as MTT reduction, was significantly reduced in the presence of 50, 100 and 2+ 200 ìM Fe . HT22 cell morphology, evaluated by phase-contrast microscopy, showed evident morphological alterations including rounded cell body with a decreased number of cell projections. The decrease in MTT reduction strongly correlated with the changes in cellular morphology. Based on these data we defined that 24-h exposure to iron (25 and 50 ìM) caused a mild oxidative injury. Under these experimental conditions both Akt and GSK3â phosphorylation were increased. We conclude that iron-induced neurotoxicity activates Akt promoting GSK3â inhibition under mild oxidative injury in hippocampal neurons.
publishDate 2010
dc.date.none.fl_str_mv 2010
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/11336/223463
Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons; XLVI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Puerto Madryn; Argentina; 2010; 74-74
0327-9545
1667-5746
CONICET Digital
CONICET
url http://hdl.handle.net/11336/223463
identifier_str_mv Akt/GSK3beta signaling during iron-induced neurotoxicity in HT22 hippocampal neurons; XLVI Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Puerto Madryn; Argentina; 2010; 74-74
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/archivos/biocell-34.pdf
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 Biocell
publisher.none.fl_str_mv Biocell
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 13.13397

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