Genes involved in the balance between neuronal survival and death during inflammation

Autores
Glezer, Isaias; Chernomoretz, Ariel; David, Samuel; Plante, Marie-Michèlle; Rivest, Serge
Año de publicación
2007
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS. © 2007 Glezer et al.
Fil: Glezer, Isaias. Centre Hospitalier de L'université Laval (chul); Canadá
Fil: Chernomoretz, Ariel. Universidad de Buenos Aires; Argentina. Centre Hospitalier de L'université Laval (chul); Canadá. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; Argentina
Fil: David, Samuel. Centre Universitaire de Santé Mcgill, Institut de Recherche; Canadá
Fil: Plante, Marie-Michèlle. Centre Hospitalier de L'université Laval (chul); Canadá
Fil: Rivest, Serge. Centre Hospitalier de L'université Laval (chul); Canadá
Materia
neurodegenerative disease
gene expression
microarray analysis
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:11336/71611
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/71611
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Genes involved in the balance between neuronal survival and death during inflammationGlezer, IsaiasChernomoretz, ArielDavid, SamuelPlante, Marie-MichèlleRivest, Sergeneurodegenerative diseasegene expressionmicroarray analysishttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS. © 2007 Glezer et al.Fil: Glezer, Isaias. Centre Hospitalier de L'université Laval (chul); CanadáFil: Chernomoretz, Ariel. Universidad de Buenos Aires; Argentina. Centre Hospitalier de L'université Laval (chul); Canadá. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; ArgentinaFil: David, Samuel. Centre Universitaire de Santé Mcgill, Institut de Recherche; CanadáFil: Plante, Marie-Michèlle. Centre Hospitalier de L'université Laval (chul); CanadáFil: Rivest, Serge. Centre Hospitalier de L'université Laval (chul); CanadáPublic Library of Science2007-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/71611Glezer, Isaias; Chernomoretz, Ariel; David, Samuel; Plante, Marie-Michèlle; Rivest, Serge; Genes involved in the balance between neuronal survival and death during inflammation; Public Library of Science; Plos One; 2; 3; 12-2007; 1-101932-6203CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.plosone.org/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0000310info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0000310info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:24:32Zoai:ri.conicet.gov.ar:11336/71611instacron: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:34982025-09-10 13:24:32.33CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Genes involved in the balance between neuronal survival and death during inflammation
title Genes involved in the balance between neuronal survival and death during inflammation
spellingShingle Genes involved in the balance between neuronal survival and death during inflammation
Glezer, Isaias
neurodegenerative disease
gene expression
microarray analysis
title_short Genes involved in the balance between neuronal survival and death during inflammation
title_full Genes involved in the balance between neuronal survival and death during inflammation
title_fullStr Genes involved in the balance between neuronal survival and death during inflammation
title_full_unstemmed Genes involved in the balance between neuronal survival and death during inflammation
title_sort Genes involved in the balance between neuronal survival and death during inflammation
dc.creator.none.fl_str_mv Glezer, Isaias
Chernomoretz, Ariel
David, Samuel
Plante, Marie-Michèlle
Rivest, Serge
author Glezer, Isaias
author_facet Glezer, Isaias
Chernomoretz, Ariel
David, Samuel
Plante, Marie-Michèlle
Rivest, Serge
author_role author
author2 Chernomoretz, Ariel
David, Samuel
Plante, Marie-Michèlle
Rivest, Serge
author2_role author
author
author
author
dc.subject.none.fl_str_mv neurodegenerative disease
gene expression
microarray analysis
topic neurodegenerative disease
gene expression
microarray analysis
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS. © 2007 Glezer et al.
Fil: Glezer, Isaias. Centre Hospitalier de L'université Laval (chul); Canadá
Fil: Chernomoretz, Ariel. Universidad de Buenos Aires; Argentina. Centre Hospitalier de L'université Laval (chul); Canadá. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; Argentina
Fil: David, Samuel. Centre Universitaire de Santé Mcgill, Institut de Recherche; Canadá
Fil: Plante, Marie-Michèlle. Centre Hospitalier de L'université Laval (chul); Canadá
Fil: Rivest, Serge. Centre Hospitalier de L'université Laval (chul); Canadá
description Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS. © 2007 Glezer et al.
publishDate 2007
dc.date.none.fl_str_mv 2007-12
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/11336/71611
Glezer, Isaias; Chernomoretz, Ariel; David, Samuel; Plante, Marie-Michèlle; Rivest, Serge; Genes involved in the balance between neuronal survival and death during inflammation; Public Library of Science; Plos One; 2; 3; 12-2007; 1-10
1932-6203
CONICET Digital
CONICET
url http://hdl.handle.net/11336/71611
identifier_str_mv Glezer, Isaias; Chernomoretz, Ariel; David, Samuel; Plante, Marie-Michèlle; Rivest, Serge; Genes involved in the balance between neuronal survival and death during inflammation; Public Library of Science; Plos One; 2; 3; 12-2007; 1-10
1932-6203
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.plosone.org/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0000310
info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0000310
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
dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of Science
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_ 1842981361737007104
score 12.48226

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