| dc.contributor.author | Burguillos, MA | en_US |
| dc.contributor.author | Svensson, M | en_US |
| dc.contributor.author | Schulte, T | en_US |
| dc.contributor.author | Boza-Serrano, A | en_US |
| dc.contributor.author | Garcia-Quintanilla, A | en_US |
| dc.contributor.author | Kavanagh, E | en_US |
| dc.contributor.author | Santiago, M | en_US |
| dc.contributor.author | Viceconte, N | en_US |
| dc.contributor.author | Oliva-Martin, MJ | en_US |
| dc.contributor.author | Osman, AM | en_US |
| dc.contributor.author | Salomonsson, E | en_US |
| dc.contributor.author | Amar, L | en_US |
| dc.contributor.author | Persson, A | en_US |
| dc.contributor.author | Blomgren, K | en_US |
| dc.contributor.author | Achour, A | en_US |
| dc.contributor.author | Englund, E | en_US |
| dc.contributor.author | Leffler, H | en_US |
| dc.contributor.author | Venero, JL | en_US |
| dc.contributor.author | Joseph, B | en_US |
| dc.contributor.author | Deierborg, T | en_US |
| dc.date.accessioned | 2015-03-26T09:01:27Z | |
| dc.date.accessioned | 2015-09-08T12:49:04Z | |
| dc.date.available | 2015-02-01 | en_US |
| dc.date.issued | 2015-03-10 | en_US |
| dc.identifier.other | 10.1016/j.celrep.2015.02.012 | |
| dc.identifier.uri | http://qmro.qmul.ac.uk/xmlui/handle/123456789/8528 | |
| dc.description | This is an open access article under the CC BY-NC-ND license | en_US |
| dc.description.abstract | Inflammatory response induced by microglia plays a critical role in the demise of neuronal populations in neuroinflammatory diseases. Although the role of toll-like receptor 4 (TLR4) in microglia's inflammatory response is fully acknowledged, little is known about endogenous ligands that trigger TLR4 activation. Here, we report that galectin-3 (Gal3) released by microglia acts as an endogenous paracrine TLR4 ligand. Gal3-TLR4 interaction was further confirmed in a murine neuroinflammatory model (intranigral lipopolysaccharide [LPS] injection) and in human stroke subjects. Depletion of Gal3 exerted neuroprotective and anti-inflammatory effects following global brain ischemia and in the neuroinflammatory LPS model. These results suggest that Gal3-dependent-TLR4 activation could contribute to sustained microglia activation, prolonging the inflammatory response in the brain. | en_US |
| dc.description.sponsorship | M.A.B. is supported by postdoctoral fellowship award from Swedish Research
Council. This work has been supported by the following grants (in alphabetical
order): A.E. Berger Foundation, Bergvall Foundation, Crafoord Foundation, G.
& J. Koch Foundation, Gyllenstiernska Krapperup Foundation, Karolinska
Institute research grants, Lars Hierta Memorial Foundation, Proyecto de Excelencia
from Junta de Andalucia (CTS-6494), Royal Physiographic Society,
Royal Physiographic Society in Lund Foundation, Spanish Ministerio de Ciencia
y Tecnologı´a (SAF2009-13778), Stohnes Foundation, Swedish Cancer Society,
Swedish Research Council (grant no. 2012-2229), Swedish Parkinson
Foundation, Swedish Strategic Research Area MultiPark at Lund University,
Swedish National Stroke Foundation, and Wiberg Foundation | en_US |
| dc.format.extent | 1626 - 1638 | en_US |
| dc.language | eng | en_US |
| dc.language.iso | en | en_US |
| dc.relation.ispartof | Cell Rep | en_US |
| dc.relation.replaces | http://qmro.qmul.ac.uk/jspui/handle/123456789/7074 | |
| dc.relation.replaces | 123456789/7074 | |
| dc.title | Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation. | en_US |
| dc.type | Article | |
| dc.identifier.doi | 10.1016/j.celrep.2015.02.012 | en_US |
| pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/25753426 | en_US |
| pubs.issue | 9 | en_US |
| pubs.notes | Not known | en_US |
| pubs.publication-status | Published | en_US |
| pubs.volume | 10 | en_US |
| dcterms.dateAccepted | 2015-02-01 | en_US |
