Amyloid β1–42 Oligomers Induce Galectin–1S8 O–GlcNAcylation Leading to Microglia Migration
dc.contributor.author | Arrazola Sastre, Alazne | |
dc.contributor.author | Luque Montoro, Miriam | |
dc.contributor.author | Llavero Bernal, Francisco | |
dc.contributor.author | Zugaza Gurruchaga, José Luis | |
dc.date.accessioned | 2023-08-01T11:11:53Z | |
dc.date.available | 2023-08-01T11:11:53Z | |
dc.date.issued | 2023-07-17 | |
dc.identifier.citation | Cells 12(14) : (2023) // Article ID 1876 | es_ES |
dc.identifier.issn | 2073-4409 | |
dc.identifier.uri | http://hdl.handle.net/10810/62085 | |
dc.description.abstract | Protein O–GlcNAcylation has been associated with neurodegenerative diseases such as Alzheimer’s disease (AD). The O–GlcNAcylation of the Amyloid Precursor Protein (APP) regulates both the trafficking and the processing of the APP through the amyloidogenic pathway, resulting in the release and aggregation of the Aβ1–42 peptide. Microglia clears Aβ aggregates and dead cells to maintain brain homeostasis. Here, using LC-MS/MS, we revealed that the Aβ1–42 oligomers modify the microglia O-GlcNAcome. We identified 55 proteins, focusing our research on Galectin-1 protein since it is a very versatile protein from a functional point of view. Combining biochemical with genetic approaches, we demonstrated that Aβ1–42 oligomers specifically target Galectin–1S8 O–GlcNAcylation via OGT. In addition to this, the Gal–1–O–GlcNAcylated form, in turn, controls human microglia migration. Given the importance of microglia migration in the progression of AD, this study reports the relationship between the Aβ1–42 oligomers and Serine 8–O–GlcNAcylation of Galectin–1 to drive microglial migration. | es_ES |
dc.description.sponsorship | A.A.S. received a predoctoral fellowship (PRE_2017_1_0016) from the Basque Government. M.L.M. received a fellowship from the Foundation “Jesús de Gangoiti y Barrera”. J.L.Z. is supported by the Instituto de Salud Carlos III (PI18/00207), Basque Government (PIBA_2020_1_0048 and Elkartek Program KK-2023/00050) and University of Basque Country Grant (US19/04). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.subject | amyloid β1–42 oligomers | es_ES |
dc.subject | OGT | es_ES |
dc.subject | O-GlcNAcylation | es_ES |
dc.subject | Galectin–1 | es_ES |
dc.subject | Galectin–1Serine 8–O–GlcNAcylation | es_ES |
dc.subject | Gal–1S8A | es_ES |
dc.subject | microglia | es_ES |
dc.subject | migration | es_ES |
dc.title | Amyloid β1–42 Oligomers Induce Galectin–1S8 O–GlcNAcylation Leading to Microglia Migration | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.date.updated | 2023-07-28T12:22:13Z | |
dc.rights.holder | © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/ 4.0/). | es_ES |
dc.relation.publisherversion | https://www.mdpi.com/2073-4409/12/14/1876 | es_ES |
dc.identifier.doi | 10.3390/cells12141876 | |
dc.departamentoes | Genética, antropología física y fisiología animal | |
dc.departamentoeu | Genetika,antropologia fisikoa eta animalien fisiologia |
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Except where otherwise noted, this item's license is described as © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/ 4.0/).