PLD and PI3K signaling in neuronal oxidative stress

Autores
Salvador, Gabriela Alejandra
Año de publicación
2015
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Lipid signaling cascades have important roles in the regulation of cellular fate. Our studies provide new insights into the regulation and physiological role of lipid messengers during neuronal oxidative stress (OS). Specifically, we have studied neuronal signal events derived from phosphatidylcholine (PC) and phosphatidylinositol (PI). Synaptic OS triggers phospholipase D (PLD) activation and, consequently, a rise in phosphatidic acid and diacylglycerol (DAG) generation from PC. These lipid messengers activate downstream signaling cascades as ERK1/2 and conventional PKCs and regulate glutamate transport in the synaptic cleft of adult rat brains. Studies in aged brains reveal an increased synaptic susceptibility to OS and an impairment in the DAG-mediated signaling pathways. Tyrosine phosphorylation associated with PI phosphorylation and phosphoinositide 3 kinase (PI3K) activation are stimulated in OS-exposed hippocampal neurons and synapses. PI3K activation and its downstream effector kinase, Akt, trigger pleiotropic neuroprotective mechanisms against OS by suppressing FOXO3A transcriptional activity, inhibiting GSK3β and upregulating glutathione metabolism. In summary, we have characterized signaling events elicited by PLD and PI3K activation, which produce lipid messengers that control smart strategies for preventing neuronal death triggered by OS.
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
LI Reunion Anual de Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Mar del Plata
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Materia
PHOSPHOLIPASE D
PI3K
OXIDATIVE STRESS
NEURODEGENERATION
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:11336/237543
Acceder
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network_name_str CONICET Digital (CONICET)
spelling PLD and PI3K signaling in neuronal oxidative stressSalvador, Gabriela AlejandraPHOSPHOLIPASE DPI3KOXIDATIVE STRESSNEURODEGENERATIONhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Lipid signaling cascades have important roles in the regulation of cellular fate. Our studies provide new insights into the regulation and physiological role of lipid messengers during neuronal oxidative stress (OS). Specifically, we have studied neuronal signal events derived from phosphatidylcholine (PC) and phosphatidylinositol (PI). Synaptic OS triggers phospholipase D (PLD) activation and, consequently, a rise in phosphatidic acid and diacylglycerol (DAG) generation from PC. These lipid messengers activate downstream signaling cascades as ERK1/2 and conventional PKCs and regulate glutamate transport in the synaptic cleft of adult rat brains. Studies in aged brains reveal an increased synaptic susceptibility to OS and an impairment in the DAG-mediated signaling pathways. Tyrosine phosphorylation associated with PI phosphorylation and phosphoinositide 3 kinase (PI3K) activation are stimulated in OS-exposed hippocampal neurons and synapses. PI3K activation and its downstream effector kinase, Akt, trigger pleiotropic neuroprotective mechanisms against OS by suppressing FOXO3A transcriptional activity, inhibiting GSK3β and upregulating glutathione metabolism. In summary, we have characterized signaling events elicited by PLD and PI3K activation, which produce lipid messengers that control smart strategies for preventing neuronal death triggered by OS.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; ArgentinaLI Reunion Anual de Sociedad Argentina de Investigación en Bioquímica y Biología MolecularMar del PlataArgentinaSociedad Argentina de Investigación en Bioquímica y Biología MolecularTech Science Press2015info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/237543PLD and PI3K signaling in neuronal oxidative stress; LI Reunion Anual de Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Mar del Plata; Argentina; 2015; 27-270025-76801669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.techscience.com/biocell/v39nSuppl.S/34055/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 Técnicas2025-09-29T09:36:50Zoai:ri.conicet.gov.ar:11336/237543instacron: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 09:36:50.575CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv PLD and PI3K signaling in neuronal oxidative stress
title PLD and PI3K signaling in neuronal oxidative stress
spellingShingle PLD and PI3K signaling in neuronal oxidative stress
Salvador, Gabriela Alejandra
PHOSPHOLIPASE D
PI3K
OXIDATIVE STRESS
NEURODEGENERATION
title_short PLD and PI3K signaling in neuronal oxidative stress
title_full PLD and PI3K signaling in neuronal oxidative stress
title_fullStr PLD and PI3K signaling in neuronal oxidative stress
title_full_unstemmed PLD and PI3K signaling in neuronal oxidative stress
title_sort PLD and PI3K signaling in neuronal oxidative stress
dc.creator.none.fl_str_mv Salvador, Gabriela Alejandra
author Salvador, Gabriela Alejandra
author_facet Salvador, Gabriela Alejandra
author_role author
dc.subject.none.fl_str_mv PHOSPHOLIPASE D
PI3K
OXIDATIVE STRESS
NEURODEGENERATION
topic PHOSPHOLIPASE D
PI3K
OXIDATIVE STRESS
NEURODEGENERATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Lipid signaling cascades have important roles in the regulation of cellular fate. Our studies provide new insights into the regulation and physiological role of lipid messengers during neuronal oxidative stress (OS). Specifically, we have studied neuronal signal events derived from phosphatidylcholine (PC) and phosphatidylinositol (PI). Synaptic OS triggers phospholipase D (PLD) activation and, consequently, a rise in phosphatidic acid and diacylglycerol (DAG) generation from PC. These lipid messengers activate downstream signaling cascades as ERK1/2 and conventional PKCs and regulate glutamate transport in the synaptic cleft of adult rat brains. Studies in aged brains reveal an increased synaptic susceptibility to OS and an impairment in the DAG-mediated signaling pathways. Tyrosine phosphorylation associated with PI phosphorylation and phosphoinositide 3 kinase (PI3K) activation are stimulated in OS-exposed hippocampal neurons and synapses. PI3K activation and its downstream effector kinase, Akt, trigger pleiotropic neuroprotective mechanisms against OS by suppressing FOXO3A transcriptional activity, inhibiting GSK3β and upregulating glutathione metabolism. In summary, we have characterized signaling events elicited by PLD and PI3K activation, which produce lipid messengers that control smart strategies for preventing neuronal death triggered by OS.
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
LI Reunion Anual de Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Mar del Plata
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
description Lipid signaling cascades have important roles in the regulation of cellular fate. Our studies provide new insights into the regulation and physiological role of lipid messengers during neuronal oxidative stress (OS). Specifically, we have studied neuronal signal events derived from phosphatidylcholine (PC) and phosphatidylinositol (PI). Synaptic OS triggers phospholipase D (PLD) activation and, consequently, a rise in phosphatidic acid and diacylglycerol (DAG) generation from PC. These lipid messengers activate downstream signaling cascades as ERK1/2 and conventional PKCs and regulate glutamate transport in the synaptic cleft of adult rat brains. Studies in aged brains reveal an increased synaptic susceptibility to OS and an impairment in the DAG-mediated signaling pathways. Tyrosine phosphorylation associated with PI phosphorylation and phosphoinositide 3 kinase (PI3K) activation are stimulated in OS-exposed hippocampal neurons and synapses. PI3K activation and its downstream effector kinase, Akt, trigger pleiotropic neuroprotective mechanisms against OS by suppressing FOXO3A transcriptional activity, inhibiting GSK3β and upregulating glutathione metabolism. In summary, we have characterized signaling events elicited by PLD and PI3K activation, which produce lipid messengers that control smart strategies for preventing neuronal death triggered by OS.
publishDate 2015
dc.date.none.fl_str_mv 2015
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Reunión
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/11336/237543
PLD and PI3K signaling in neuronal oxidative stress; LI Reunion Anual de Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Mar del Plata; Argentina; 2015; 27-27
0025-7680
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/237543
identifier_str_mv PLD and PI3K signaling in neuronal oxidative stress; LI Reunion Anual de Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Mar del Plata; Argentina; 2015; 27-27
0025-7680
1669-9106
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/v39nSuppl.S/34055/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
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score 13.070432

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