Galectin-1 in myelin repair
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...
| Autores: | , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2016 |
| País: | Argentina |
| Institución: | Consejo Nacional de Investigaciones Científicas y Técnicas |
| Repositorio: | CONICET Digital (CONICET) |
| Idioma: | inglés |
| OAI Identifier: | oai:ri.conicet.gov.ar:11336/49586 |
| Acceso en línea: | http://hdl.handle.net/11336/49586 |
| Access Level: | acceso abierto |
| Palabra clave: | DEMYELINATION-REMYELINATION GALECTIN-1 LYSOLECITHIN MICROGLIA NEUROSCIENCE PHAGOCYTOSIS https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| Sumario: | 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, |
|---|