Please use this identifier to cite or link to this item: http://repositorio.ufla.br/jspui/handle/1/48128
Title: IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
Keywords: Wnt signaling pathway
Fibroblast-like synoviocytes
Rheumatoid arthritis
Spondyloarthritis
Via de sinalização da Wnt
Sinoviócitos semelhantes a fibroblastos
Artrite reumatóide
Espondiloartrites
Doenças inflamatórias
Issue Date: Aug-2020
Publisher: Associação Brasileira de Divulgação Científica
Citation: RESENDE, G. G. et al. IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases. Brazilian Journal of Medical and Biological Research, Ribeirão Preto, v. 53, n. 9, e9880, 2020. DOI: http://dx.doi.org/10.1590/1414-431X20209880.
Abstract: Rheumatoid 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-α), 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- α, 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; P<0.01) 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.
URI: http://repositorio.ufla.br/jspui/handle/1/48128
Appears in Collections:DES - Artigos publicados em periódicos

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