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dc.contributor.authorKabala, P. A.
dc.contributor.authorMalvar-Fernandez, B.
dc.contributor.authorLopes, A. P.
dc.contributor.authorCarvalheiro, T.
dc.contributor.authorHartgring, S. A. Y.
dc.contributor.authorTang, M. W.
dc.contributor.authorConde Muro, Carmen 
dc.contributor.authorBaeten, D. L.
dc.contributor.authorSleeman, M.
dc.contributor.authorTak, P. P.
dc.contributor.authorConnor, J.
dc.contributor.authorRadstake, T. R.
dc.contributor.authorReedquist, K. A.
dc.contributor.authorGarcia, S.
dc.date.accessioned2022-04-29T10:28:40Z
dc.date.available2022-04-29T10:28:40Z
dc.date.issued2020
dc.identifier.issn1462-0324
dc.identifier.otherhttps://www.ncbi.nlm.nih.gov/pubmed/31377797es
dc.identifier.urihttp://hdl.handle.net/20.500.11940/16639
dc.description.abstractOBJECTIVE: To examine the role of Tie2 signalling in macrophage activation within the context of the inflammatory synovial microenvironment present in patients with RA and PsA. METHODS: Clinical responses and macrophage function were examined in wild-type and Tie2-overexpressing (Tie2-TG) mice in the K/BxN serum transfer model of arthritis. Macrophages derived from peripheral blood monocytes from healthy donors, RA and PsA patients, and RA and PsA synovial tissue explants were stimulated with TNF (10 ng/ml), angiopoietin (Ang)-1 or Ang-2 (200 ng/ml), or incubated with an anti-Ang2 neutralizing antibody. mRNA and protein expression of inflammatory mediators was analysed by quantitative PCR, ELISA and Luminex. RESULTS: Tie2-TG mice displayed more clinically severe arthritis than wild-type mice, accompanied by enhanced joint expression of IL6, IL12B, NOS2, CCL2 and CXCL10, and activation of bone marrow-derived macrophages in response to Ang-2 stimulation. Ang-1 and Ang-2 significantly enhanced TNF-induced expression of pro-inflammatory cytokines and chemokines in macrophages from healthy donors differentiated with RA and PsA SF and peripheral blood-derived macrophages from RA and PsA patients. Both Ang-1 and Ang-2 induced the production of IL-6, IL-12p40, IL-8 and CCL-3 in synovial tissue explants of RA and PsA patients, and Ang-2 neutralization suppressed the production of IL-6 and IL-8 in the synovial tissue of RA patients. CONCLUSION: Tie2 signalling enhances TNF-dependent activation of macrophages within the context of ongoing synovial inflammation in RA and PsA, and neutralization of Tie2 ligands might be a promising therapeutic target in the treatment of these diseases.en
dc.rightsAtribución-NoComercial 4.0 Internacional
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.subject.meshMacrophage Activation*
dc.subject.meshHumans*
dc.subject.meshCytokines*
dc.subject.meshMacrophages*
dc.subject.meshSynovial Fluid*
dc.subject.meshMice*
dc.subject.meshSynovial Membrane*
dc.subject.meshSignal Transduction*
dc.subject.meshArthritis*
dc.subject.meshAnimals*
dc.subject.meshInflammation*
dc.titlePromotion of macrophage activation by Tie2 in the context of the inflamed synovia of rheumatoid arthritis and psoriatic arthritis patientsen
dc.typeJournal Articlees
dc.authorsophosKabala, P. A.;Malvar-Fernandez, B.;Lopes, A. P.;Carvalheiro, T.;Hartgring, S. A. Y.;Tang, M. W.;Conde, C.;Baeten, D. L.;Sleeman, M.;Tak, P. P.;Connor, J.;Radstake, T. R.;Reedquist, K. A.;Garcia, S.
dc.identifier.doi10.1093/rheumatology/kez315
dc.identifier.pmid31377797
dc.identifier.sophos39761
dc.issue.number2es
dc.journal.titleRHEUMATOLOGYes
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Santiago de Compostela - Complexo Hospitalario Universitario de Santiago de Compostela::Reumatoloxíaes
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS)es
dc.page.initial426es
dc.page.final438es
dc.rights.accessRightsopenAccess
dc.subject.decslíquido sinovial*
dc.subject.decsanimales*
dc.subject.decsmembrana sinovial*
dc.subject.decscitocinas*
dc.subject.decshumanos*
dc.subject.decsinflamación*
dc.subject.decstransducción de señales*
dc.subject.decsmacrófagos*
dc.subject.decsratones*
dc.subject.decsactivación de macrófagos*
dc.subject.decsartritis*
dc.subject.keywordCHUSes
dc.subject.keywordIDISes
dc.typefidesArtículo Originales
dc.typesophosArtículo Originales
dc.volume.number59es


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