1. Repositório Institucional da UFMG
  2. Publicações Científicas e Culturais
  3. Artigo de Periódico
Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/62070
Full metadata record
DC FieldValueLanguage
dc.creatorGustavo Gomes Resendept_BR
dc.creatorCamilla Ribeiro Lima Machadopt_BR
dc.creatorM.a. Rochapt_BR
dc.creatorRbv Macedopt_BR
dc.creatorAdriana Maria Kakehasipt_BR
dc.creatorMarcus Vinícius Melo de Andradept_BR
dc.date.accessioned2023-12-18T23:42:29Z-
dc.date.available2023-12-18T23:42:29Z-
dc.date.issued2020-
dc.citation.volume53pt_BR
dc.citation.issue9pt_BR
dc.citation.spagee9880pt_BR
dc.citation.epagee9885pt_BR
dc.identifier.doi10.1590/1414-431X20209880pt_BR
dc.identifier.issn0100879Xpt_BR
dc.identifier.urihttp://hdl.handle.net/1843/62070-
dc.description.resumoRheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) are inflammatory diseases with different bone remodeling patterns. Fibroblast-like synoviocytes (FLS) are cells involved in the transition from an acute and reparable phase to a chronic and persistent stage in these diseases. The distinction of joint phenotypes involves inflammatory cytokines such as tumor necrosis factor alpha (TNF-a), interleukin (IL)-17, and IL-22 directly or through key signaling pathways such as Wnt. To evaluate the role of FLS as the source of Wnt antagonists (sFRP3/FRZB and Dkk1) in the synovia, levels of TNF- a, IL-17, IL-22, Dkk1, and sFRP3 were measured by ELISA directly in the synovial fluid of patients with RA, PsA, or AS. Dkk1 and sFRP3 were also measured in the FLS culture supernatants after different inflammatory stimulus. sFRP3 and Dkk1 are constitutively expressed by FLS. IL-22 and sFRP3 were positively correlated (r=0.76; Po0.01) in synovial fluid. The stimulation of FLS with IL-22, but not TNF-alpha and IL-17, increased the production of sFRP3. No stimulus altered the basal expression of Dkk1. These results showed, for the first time, the ability of IL-22 to increase the expression of sFRP3/FRZB by human FLS in both in vitro and ex vivo models. This finding linked IL-22 to local inhibition of Wnt signaling and possibly to blockade of osteogenesis. Furthermore, FLS presented as a source of this inhibitor in synovial fluid, assigning to this cell a bone injury mechanism.pt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentMED - DEPARTAMENTO DE APARELHO LOCOMOTORpt_BR
dc.publisher.departmentMED - DEPARTAMENTO DE CLÍNICA MÉDICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofBrazilian Journal of Medical and Biological Research-
dc.rightsAcesso Abertopt_BR
dc.subjectL-22pt_BR
dc.subjectWnt Signaling Pathwaypt_BR
dc.subjectFibroblast-like synoviocytespt_BR
dc.subjectRheumatoid arthritispt_BR
dc.subjectSpondyloarthritispt_BR
dc.subject.otherWnt Signaling Pathwaypt_BR
dc.subject.otherArthritis, Rheumatoidpt_BR
dc.titleIl-22 increases the production of sfrp3 by fls in inflammatory joint diseasespt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://doi.org/10.1590/1414-431X20209880pt_BR
Appears in Collections:Artigo de Periódico

Files in This Item:
File Description SizeFormat 
IL-22 increases the production of sFRP3 by FLS in pdfa.pdf290.15 kBAdobe PDFView/Open
Show simple item record


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.