Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights
- Autores
- Uranga, Romina Maria; Antollini, Silvia Susana; Salvador, Gabriela Alejandra
- Año de publicación
- 2014
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- We have previously demonstrated that oligomeric amyloid β peptide (oAβ), known as the most harmful species of Aβ, concomitant with iron overload led to synaptic injury and local activation of several signaling cascades. In this work, we characterized hippocampal neuronal response to oAβ exposure both in the presence and absence of iron. HT22 neurons exposed to iron overload displayed increased lipid peroxidation, slight loss of mitochondrial function, and activation of ERK and Akt pathways. oAβ neither induced an increase in lipid peroxidation nor altered mitochondrial function. However, oAβ alone triggered the activation of ERK and Akt, and the coincubation with oAβ/iron restored pAkt and pERK to the control levels. In addition, we also studied the effect of iron, oAβ and both conditions together, on the biophysical state of the plasma membrane by measuring the generalized polarization of the fluorescence probe Laurdan and the fluorescence anisotropy of DPH and TMA-DPH. Both studies showed that the presence of iron (even at the highest concentration tested), oAβ, or both conditions together, did not perturb the lipid order of the membrane. We conclude that oAβ activates signaling pathways in the absence of oxidative stress or membrane disturbances 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: Antollini, Silvia Susana. 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
L Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Rosario
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular - Materia
-
NEURODEGENERATION
AMYLOID PEPTIDE
HIPPOCAMPUS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/235389
Ver los metadatos del registro completo
id |
CONICETDig_5df82da5e8da12918349b4bd5c1dca27 |
---|---|
oai_identifier_str |
oai:ri.conicet.gov.ar:11336/235389 |
network_acronym_str |
CONICETDig |
repository_id_str |
3498 |
network_name_str |
CONICET Digital (CONICET) |
spelling |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insightsUranga, Romina MariaAntollini, Silvia SusanaSalvador, Gabriela AlejandraNEURODEGENERATIONAMYLOID PEPTIDEHIPPOCAMPUShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1We have previously demonstrated that oligomeric amyloid β peptide (oAβ), known as the most harmful species of Aβ, concomitant with iron overload led to synaptic injury and local activation of several signaling cascades. In this work, we characterized hippocampal neuronal response to oAβ exposure both in the presence and absence of iron. HT22 neurons exposed to iron overload displayed increased lipid peroxidation, slight loss of mitochondrial function, and activation of ERK and Akt pathways. oAβ neither induced an increase in lipid peroxidation nor altered mitochondrial function. However, oAβ alone triggered the activation of ERK and Akt, and the coincubation with oAβ/iron restored pAkt and pERK to the control levels. In addition, we also studied the effect of iron, oAβ and both conditions together, on the biophysical state of the plasma membrane by measuring the generalized polarization of the fluorescence probe Laurdan and the fluorescence anisotropy of DPH and TMA-DPH. Both studies showed that the presence of iron (even at the highest concentration tested), oAβ, or both conditions together, did not perturb the lipid order of the membrane. We conclude that oAβ activates signaling pathways in the absence of oxidative stress or membrane disturbances 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: Antollini, Silvia Susana. 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; ArgentinaL Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología MolecularRosarioArgentinaSociedad Argentina de Investigación en Bioquímica y Biología MolecularTech Science Press2014info: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/11336/235389Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights; L Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Rosario; Argentina; 2014; 112-1120327-9545CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.techscience.com/biocell/v38nSuppl.S/34067/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 Técnicas2025-09-03T10:02:17Zoai:ri.conicet.gov.ar:11336/235389instacron: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 10:02:17.586CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
title |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
spellingShingle |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights Uranga, Romina Maria NEURODEGENERATION AMYLOID PEPTIDE HIPPOCAMPUS |
title_short |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
title_full |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
title_fullStr |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
title_full_unstemmed |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
title_sort |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights |
dc.creator.none.fl_str_mv |
Uranga, Romina Maria Antollini, Silvia Susana Salvador, Gabriela Alejandra |
author |
Uranga, Romina Maria |
author_facet |
Uranga, Romina Maria Antollini, Silvia Susana Salvador, Gabriela Alejandra |
author_role |
author |
author2 |
Antollini, Silvia Susana Salvador, Gabriela Alejandra |
author2_role |
author author |
dc.subject.none.fl_str_mv |
NEURODEGENERATION AMYLOID PEPTIDE HIPPOCAMPUS |
topic |
NEURODEGENERATION AMYLOID PEPTIDE HIPPOCAMPUS |
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 that oligomeric amyloid β peptide (oAβ), known as the most harmful species of Aβ, concomitant with iron overload led to synaptic injury and local activation of several signaling cascades. In this work, we characterized hippocampal neuronal response to oAβ exposure both in the presence and absence of iron. HT22 neurons exposed to iron overload displayed increased lipid peroxidation, slight loss of mitochondrial function, and activation of ERK and Akt pathways. oAβ neither induced an increase in lipid peroxidation nor altered mitochondrial function. However, oAβ alone triggered the activation of ERK and Akt, and the coincubation with oAβ/iron restored pAkt and pERK to the control levels. In addition, we also studied the effect of iron, oAβ and both conditions together, on the biophysical state of the plasma membrane by measuring the generalized polarization of the fluorescence probe Laurdan and the fluorescence anisotropy of DPH and TMA-DPH. Both studies showed that the presence of iron (even at the highest concentration tested), oAβ, or both conditions together, did not perturb the lipid order of the membrane. We conclude that oAβ activates signaling pathways in the absence of oxidative stress or membrane disturbances 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: Antollini, Silvia Susana. 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 L Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular Rosario Argentina Sociedad Argentina de Investigación en Bioquímica y Biología Molecular |
description |
We have previously demonstrated that oligomeric amyloid β peptide (oAβ), known as the most harmful species of Aβ, concomitant with iron overload led to synaptic injury and local activation of several signaling cascades. In this work, we characterized hippocampal neuronal response to oAβ exposure both in the presence and absence of iron. HT22 neurons exposed to iron overload displayed increased lipid peroxidation, slight loss of mitochondrial function, and activation of ERK and Akt pathways. oAβ neither induced an increase in lipid peroxidation nor altered mitochondrial function. However, oAβ alone triggered the activation of ERK and Akt, and the coincubation with oAβ/iron restored pAkt and pERK to the control levels. In addition, we also studied the effect of iron, oAβ and both conditions together, on the biophysical state of the plasma membrane by measuring the generalized polarization of the fluorescence probe Laurdan and the fluorescence anisotropy of DPH and TMA-DPH. Both studies showed that the presence of iron (even at the highest concentration tested), oAβ, or both conditions together, did not perturb the lipid order of the membrane. We conclude that oAβ activates signaling pathways in the absence of oxidative stress or membrane disturbances in hippocampal neurons. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014 |
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/11336/235389 Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights; L Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Rosario; Argentina; 2014; 112-112 0327-9545 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/235389 |
identifier_str_mv |
Hippocampal neuronal response to amyloid β peptide oligomers. Biological and biophysical insights; L Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Rosario; Argentina; 2014; 112-112 0327-9545 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://www.techscience.com/biocell/v38nSuppl.S/34067/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 |
Tech Science Press |
publisher.none.fl_str_mv |
Tech Science Press |
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_ |
1842269749080227840 |
score |
13.13397 |