Il-22 increases the production of sfrp3 by fls in inflammatory joint diseases

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dc.creatorGustavo Gomes Resende
dc.creatorCamilla Ribeiro Lima Machado
dc.creatorM.a. Rocha
dc.creatorRbv Macedo
dc.creatorAdriana Maria Kakehasi
dc.creatorMarcus Vinícius Melo de Andrade
dc.date.accessioned2023-12-18T23:42:29Z
dc.date.accessioned2025-09-09T00:39:30Z
dc.date.available2023-12-18T23:42:29Z
dc.date.issued2020
dc.format.mimetypepdf
dc.identifier.doi10.1590/1414-431X20209880
dc.identifier.issn0100879X
dc.identifier.urihttps://hdl.handle.net/1843/62070
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofBrazilian Journal of Medical and Biological Research
dc.rightsAcesso Aberto
dc.subjectWnt Signaling Pathway
dc.subjectArthritis, Rheumatoid
dc.subject.otherL-22
dc.subject.otherWnt Signaling Pathway
dc.subject.otherFibroblast-like synoviocytes
dc.subject.otherRheumatoid arthritis
dc.subject.otherSpondyloarthritis
dc.titleIl-22 increases the production of sfrp3 by fls in inflammatory joint diseases
dc.typeArtigo de periódico
local.citation.epagee9885
local.citation.issue9
local.citation.spagee9880
local.citation.volume53
local.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.
local.publisher.countryBrasil
local.publisher.departmentMED - DEPARTAMENTO DE APARELHO LOCOMOTOR
local.publisher.departmentMED - DEPARTAMENTO DE CLÍNICA MÉDICA
local.publisher.initialsUFMG
local.url.externahttps://doi.org/10.1590/1414-431X20209880

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