Galectin-1 in myelin repair

Autores
Rinaldi, Mariana; Thomas, Laura; Pasquini, Laura Andrea
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Galectin-1 (Gal-1) is a member of a highly conserved family of animal lectins which binds to the common disaccharide [Galβ(1-4)-GlcNAc] on both N- and O-glycans decorating cell surface glycoconjugates. Current evidence supports a role for Gal-1 in the pathophysiology of multiple sclerosis (MS), one of the most prevalent chronic inflammatory diseases, as approximately one third of MS patients generate high titres of anti-Gal-1 antibodies. Four different lesion types have been described in MS: pattern-1 and -2 lesions are thought to be mediated by the autoimmune response, while pattern-3 and -4 lesions are considered primary oligodendropathy. The first two types are experimentally simulated in mice by experimental autoimmune encephalomyelitis (EAE), while the second two are mimicked by toxic models such as cuprizone (CPZ) or lysolecithin (LPC) administration. Studies in EAE models have demonstrated that Gal-1 is highly expressed in the acute phase of the disease and that its deficiency leads to severe inflammation-induced neurodegeneration [1]. Regarding its mechanism of action,
Fil: Rinaldi, Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Thomas, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Pasquini, Laura Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Materia
DEMYELINATION-REMYELINATION
GALECTIN-1
LYSOLECITHIN
MICROGLIA
NEUROSCIENCE
PHAGOCYTOSIS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/49586
Acceder
id CONICETDig_55436d1466dcebeac1c9d89b88aeebf2
oai_identifier_str oai:ri.conicet.gov.ar:11336/49586
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Galectin-1 in myelin repairRinaldi, MarianaThomas, LauraPasquini, Laura AndreaDEMYELINATION-REMYELINATIONGALECTIN-1LYSOLECITHINMICROGLIANEUROSCIENCEPHAGOCYTOSIShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Galectin-1 (Gal-1) is a member of a highly conserved family of animal lectins which binds to the common disaccharide [Galβ(1-4)-GlcNAc] on both N- and O-glycans decorating cell surface glycoconjugates. Current evidence supports a role for Gal-1 in the pathophysiology of multiple sclerosis (MS), one of the most prevalent chronic inflammatory diseases, as approximately one third of MS patients generate high titres of anti-Gal-1 antibodies. Four different lesion types have been described in MS: pattern-1 and -2 lesions are thought to be mediated by the autoimmune response, while pattern-3 and -4 lesions are considered primary oligodendropathy. The first two types are experimentally simulated in mice by experimental autoimmune encephalomyelitis (EAE), while the second two are mimicked by toxic models such as cuprizone (CPZ) or lysolecithin (LPC) administration. Studies in EAE models have demonstrated that Gal-1 is highly expressed in the acute phase of the disease and that its deficiency leads to severe inflammation-induced neurodegeneration [1]. Regarding its mechanism of action,Fil: Rinaldi, Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Thomas, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Pasquini, Laura Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaImpact Journals2016-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/49586Rinaldi, Mariana; Thomas, Laura; Pasquini, Laura Andrea; Galectin-1 in myelin repair; Impact Journals; Oncotarget; 7; 50; 12-2016; 81979-819801949-2553CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=13455info:eu-repo/semantics/altIdentifier/doi/10.18632/oncotarget.13455info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:05:44Zoai:ri.conicet.gov.ar:11336/49586instacron: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 13:05:44.374CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Galectin-1 in myelin repair
title Galectin-1 in myelin repair
spellingShingle Galectin-1 in myelin repair
Rinaldi, Mariana
DEMYELINATION-REMYELINATION
GALECTIN-1
LYSOLECITHIN
MICROGLIA
NEUROSCIENCE
PHAGOCYTOSIS
title_short Galectin-1 in myelin repair
title_full Galectin-1 in myelin repair
title_fullStr Galectin-1 in myelin repair
title_full_unstemmed Galectin-1 in myelin repair
title_sort Galectin-1 in myelin repair
dc.creator.none.fl_str_mv Rinaldi, Mariana
Thomas, Laura
Pasquini, Laura Andrea
author Rinaldi, Mariana
author_facet Rinaldi, Mariana
Thomas, Laura
Pasquini, Laura Andrea
author_role author
author2 Thomas, Laura
Pasquini, Laura Andrea
author2_role author
author
dc.subject.none.fl_str_mv DEMYELINATION-REMYELINATION
GALECTIN-1
LYSOLECITHIN
MICROGLIA
NEUROSCIENCE
PHAGOCYTOSIS
topic DEMYELINATION-REMYELINATION
GALECTIN-1
LYSOLECITHIN
MICROGLIA
NEUROSCIENCE
PHAGOCYTOSIS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Galectin-1 (Gal-1) is a member of a highly conserved family of animal lectins which binds to the common disaccharide [Galβ(1-4)-GlcNAc] on both N- and O-glycans decorating cell surface glycoconjugates. Current evidence supports a role for Gal-1 in the pathophysiology of multiple sclerosis (MS), one of the most prevalent chronic inflammatory diseases, as approximately one third of MS patients generate high titres of anti-Gal-1 antibodies. Four different lesion types have been described in MS: pattern-1 and -2 lesions are thought to be mediated by the autoimmune response, while pattern-3 and -4 lesions are considered primary oligodendropathy. The first two types are experimentally simulated in mice by experimental autoimmune encephalomyelitis (EAE), while the second two are mimicked by toxic models such as cuprizone (CPZ) or lysolecithin (LPC) administration. Studies in EAE models have demonstrated that Gal-1 is highly expressed in the acute phase of the disease and that its deficiency leads to severe inflammation-induced neurodegeneration [1]. Regarding its mechanism of action,
Fil: Rinaldi, Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Thomas, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Pasquini, Laura Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
description Galectin-1 (Gal-1) is a member of a highly conserved family of animal lectins which binds to the common disaccharide [Galβ(1-4)-GlcNAc] on both N- and O-glycans decorating cell surface glycoconjugates. Current evidence supports a role for Gal-1 in the pathophysiology of multiple sclerosis (MS), one of the most prevalent chronic inflammatory diseases, as approximately one third of MS patients generate high titres of anti-Gal-1 antibodies. Four different lesion types have been described in MS: pattern-1 and -2 lesions are thought to be mediated by the autoimmune response, while pattern-3 and -4 lesions are considered primary oligodendropathy. The first two types are experimentally simulated in mice by experimental autoimmune encephalomyelitis (EAE), while the second two are mimicked by toxic models such as cuprizone (CPZ) or lysolecithin (LPC) administration. Studies in EAE models have demonstrated that Gal-1 is highly expressed in the acute phase of the disease and that its deficiency leads to severe inflammation-induced neurodegeneration [1]. Regarding its mechanism of action,
publishDate 2016
dc.date.none.fl_str_mv 2016-12
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/11336/49586
Rinaldi, Mariana; Thomas, Laura; Pasquini, Laura Andrea; Galectin-1 in myelin repair; Impact Journals; Oncotarget; 7; 50; 12-2016; 81979-81980
1949-2553
CONICET Digital
CONICET
url http://hdl.handle.net/11336/49586
identifier_str_mv Rinaldi, Mariana; Thomas, Laura; Pasquini, Laura Andrea; Galectin-1 in myelin repair; Impact Journals; Oncotarget; 7; 50; 12-2016; 81979-81980
1949-2553
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.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=13455
info:eu-repo/semantics/altIdentifier/doi/10.18632/oncotarget.13455
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Impact Journals
publisher.none.fl_str_mv Impact Journals
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_ 1842980219463401472
score 12.993085

Publicaciones similares