IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases

Detalhes bibliográficos
Autor(a) principal: Resende, G. G.
Data de Publicação: 2020
Outros Autores: Machado, C. R. L., Rocha, M. A., Macedo, R. B. V., Bueno Filho, J. S. S., Kakehasi, A. M., Andrade, M. V.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFLA
Texto Completo: http://repositorio.ufla.br/jspui/handle/1/48128
Resumo: 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.
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spelling IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseasesWnt signaling pathwayFibroblast-like synoviocytesRheumatoid arthritisSpondyloarthritisVia de sinalização da WntSinoviócitos semelhantes a fibroblastosArtrite reumatóideEspondiloartritesDoenças inflamatóriasRheumatoid 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.Associação Brasileira de Divulgação Científica2021-09-14T18:59:38Z2021-09-14T18:59:38Z2020-08info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfRESENDE, 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.http://repositorio.ufla.br/jspui/handle/1/48128Brazilian Journal of Medical and Biological Researchreponame:Repositório Institucional da UFLAinstname:Universidade Federal de Lavras (UFLA)instacron:UFLAhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessResende, G. G.Machado, C. R. L.Rocha, M. A.Macedo, R. B. V.Bueno Filho, J. S. S.Kakehasi, A. M.Andrade, M. V.eng2023-05-19T18:53:17Zoai:localhost:1/48128Repositório InstitucionalPUBhttp://repositorio.ufla.br/oai/requestnivaldo@ufla.br || repositorio.biblioteca@ufla.bropendoar:2023-05-19T18:53:17Repositório Institucional da UFLA - Universidade Federal de Lavras (UFLA)false
dc.title.none.fl_str_mv IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
title IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
spellingShingle IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
Resende, G. G.
Wnt signaling pathway
Fibroblast-like synoviocytes
Rheumatoid arthritis
Spondyloarthritis
Via de sinalização da Wnt
Sinoviócitos semelhantes a fibroblastos
Artrite reumatóide
Espondiloartrites
Doenças inflamatórias
title_short IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
title_full IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
title_fullStr IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
title_full_unstemmed IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
title_sort IL-22 increases the production of sFRP3 by FLS in inflammatory joint diseases
author Resende, G. G.
author_facet Resende, G. G.
Machado, C. R. L.
Rocha, M. A.
Macedo, R. B. V.
Bueno Filho, J. S. S.
Kakehasi, A. M.
Andrade, M. V.
author_role author
author2 Machado, C. R. L.
Rocha, M. A.
Macedo, R. B. V.
Bueno Filho, J. S. S.
Kakehasi, A. M.
Andrade, M. V.
author2_role author
author
author
author
author
author
dc.contributor.author.fl_str_mv Resende, G. G.
Machado, C. R. L.
Rocha, M. A.
Macedo, R. B. V.
Bueno Filho, J. S. S.
Kakehasi, A. M.
Andrade, M. V.
dc.subject.por.fl_str_mv Wnt signaling pathway
Fibroblast-like synoviocytes
Rheumatoid arthritis
Spondyloarthritis
Via de sinalização da Wnt
Sinoviócitos semelhantes a fibroblastos
Artrite reumatóide
Espondiloartrites
Doenças inflamatórias
topic Wnt signaling pathway
Fibroblast-like synoviocytes
Rheumatoid arthritis
Spondyloarthritis
Via de sinalização da Wnt
Sinoviócitos semelhantes a fibroblastos
Artrite reumatóide
Espondiloartrites
Doenças inflamatórias
description 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.
publishDate 2020
dc.date.none.fl_str_mv 2020-08
2021-09-14T18:59:38Z
2021-09-14T18:59:38Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv 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.
http://repositorio.ufla.br/jspui/handle/1/48128
identifier_str_mv 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.
url http://repositorio.ufla.br/jspui/handle/1/48128
dc.language.iso.fl_str_mv eng
language eng
dc.rights.driver.fl_str_mv http://creativecommons.org/licenses/by/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
dc.source.none.fl_str_mv Brazilian Journal of Medical and Biological Research
reponame:Repositório Institucional da UFLA
instname:Universidade Federal de Lavras (UFLA)
instacron:UFLA
instname_str Universidade Federal de Lavras (UFLA)
instacron_str UFLA
institution UFLA
reponame_str Repositório Institucional da UFLA
collection Repositório Institucional da UFLA
repository.name.fl_str_mv Repositório Institucional da UFLA - Universidade Federal de Lavras (UFLA)
repository.mail.fl_str_mv nivaldo@ufla.br || repositorio.biblioteca@ufla.br
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