Galectin-8 binds specific beta 1 integrins and induces polarized spreading highlighted by asymmetric lamellipodia in Jurkat T cells

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dc.contributor.authorCarcamo, C
dc.contributor.authorPardo, E
dc.contributor.authorOyanadel, C
dc.contributor.authorBravo Zehnder, M
dc.contributor.authorBull, P
dc.contributor.authorCaceres, M
dc.contributor.authorMartinez, J
dc.contributor.authorMassardo, L
dc.contributor.authorJacobelli, S
dc.contributor.authorGonzalez, A
dc.contributor.authorSoza, A
dc.date.accessioned2024-01-10T12:05:39Z
dc.date.available2024-01-10T12:05:39Z
dc.date.issued2006
dc.description.abstractIntegrin-mediated encounters of T cells with extracellular cues lead these cells to adhere to a variety of substrates and acquire a spread phenotype needed for their tissue incursions. We studied the effects of galectin-8 (Gal-8), beta-galactoside binding lectin, on Jurkat T cells. Immobilized Gal-8 bound alpha 1 beta 1 and alpha 5 beta 1 but not alpha 2 beta 1 and alpha 4 beta 1 and adhered these cells with similar kinetics to immobilized fibronectin (FN). Function-blocking experiments with monoclonal anti-integrin antibodies suggested that alpha 5 beta 1 is the main mediator of cell adhesion to this lectin. Gal-8, but not FN, induced extensive cell spreading frequently leading to a polarized phenotype characterized by an asymmetric lamellipodial protrusion. These morphological changes involved actin cytoskeletal rearrangements controlled by PI3K, Rac-1 and ERK1/2 activity. Gal-8-induced Rac-1 activation and binding to alpha 1 and alpha 5 integrins have not been described in any other cellular system. Strikingly, Gal-8 was also a strong stimulus on Jurkat cells in suspension, triggering ERK1/2 activation that in most adherent cells is instead dependent on cell attachment. In addition, we found that patients with systemic lupus erythematosus (SLE), a prototypic autoimmune disorder, produce Gal-8 autoantibodies that impede both its binding to integrins and cell adhesion. These are the first function-blocking autoantibodies reported for a member of the galectin family. These results indicate that Gal-8 constitutes a novel extracellular stimulus for T cells, able to bind specific beta 1 integrins and to trigger signaling pathways conducive to cell spreading. Gal-8 could modulate a wide range of T cell-driven immune processes that eventually become altered in autoimmune disorders. (C) 2005 Elsevier Inc. All rights reserved.
dc.fechaingreso.objetodigital16-04-2024
dc.format.extent13 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.yexcr.2005.10.025
dc.identifier.eissn1090-2422
dc.identifier.issn0014-4827
dc.identifier.pubmedidMEDLINE:16368432
dc.identifier.urihttps://doi.org/10.1016/j.yexcr.2005.10.025
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76047
dc.identifier.wosidWOS:000234461600002
dc.information.autorucCiencias Biológicas;Bull P;S/I;99734
dc.information.autorucMedicina;González A;S/I;52306
dc.information.autorucMedicina;Massardo M;S/I;100068
dc.information.autorucMedicina;Soza A;S/I;129570
dc.issue.numero4
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final386
dc.pagina.inicio374
dc.publisherELSEVIER INC
dc.revistaEXPERIMENTAL CELL RESEARCH
dc.rightsacceso restringido
dc.subjectgalectin-8
dc.subjectbeta 1-integrins
dc.subjectT cell spreading
dc.subjectlamellipodia
dc.subjectPI3K
dc.subjectERK
dc.subjectRac-1
dc.subjectPROTEIN-KINASE-A
dc.subjectPHOSPHATIDYLINOSITOL 3-KINASE
dc.subjectEXTRACELLULAR-MATRIX
dc.subjectALPHA-3-BETA-1 INTEGRIN
dc.subjectSIGNAL-TRANSDUCTION
dc.subjectMAP KINASES
dc.subjectACTIVATION
dc.subjectMIGRATION
dc.subjectADHESION
dc.subjectLYMPHOCYTES
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleGalectin-8 binds specific beta 1 integrins and induces polarized spreading highlighted by asymmetric lamellipodia in Jurkat T cells
dc.typeartículo
dc.volumen312
sipa.codpersvinculados99734
sipa.codpersvinculados52306
sipa.codpersvinculados100068
sipa.codpersvinculados129570
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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