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Effect of tumor necrosis factor inhibitor therapy on osteoclasts precursors in rheumatoid arthritis

2017Artigo científico Acesso aberto
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dc.contributor.authorPerpétuo, Inês Pedro
dc.contributor.authorCaetano-Lopes, Joana
dc.contributor.authorRodrigues, Ana Maria
dc.contributor.authorCampanilho-Marques, Raquel
dc.contributor.authorPonte, Cristina
dc.contributor.authorCanhao, Helena
dc.contributor.authorAinola, Mari
dc.contributor.authorFonseca, João Eurico
dc.date.accessioned2022-02-18T15:40:46Z
dc.date.available2022-02-18T15:40:46Z
dc.date.issued2017
dc.descriptionCopyright © 2017 Inês P. Perpétuo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.pt_PT
dc.description.abstractObjective. Tumor necrosis factor (TNF) increases circulating osteoclast (OC) precursors numbers by promoting their proliferation and differentiation. The aim of this study was to assess the effect of TNF inhibitors (TNFi) on the differentiation and activity of OC in rheumatoid arthritis (RA) patients. Methods. Seventeen RA patients treated with TNFi were analyzed at baseline and after a minimum follow-up period of 6 months. Blood samples were collected to assess receptor activator of nuclear factor kappa-B ligand (RANKL) surface expression on circulating leukocytes and frequency and phenotype of monocyte subpopulations. Quantification of serum levels of bone turnover markers, in vitro OC differentiation assays, and qRT-PCR for OC specific genes was performed. Results. After TNFi therapy, patients had reduced RANKL surface expression in B-lymphocytes and the frequency of circulating classical CD14brightCD16- monocytes was decreased. Serum levels of sRANKL, sRANKL/OPG ratio, and CTX-I were reduced in RA patients after TNFi treatment. Moreover, after exposure to TNFi, osteoclast differentiation and activity were decreased, as well as the expression of TRAF6 and cathepsin K. Conclusion. We propose that TNFi arrests bone loss and erosion, through two pathways: direct reduction of osteoclast precursor numbers and inhibition of intracellular signaling pathways acting through TRAF6.pt_PT
dc.description.sponsorshipThis work was supported by Fundação para a Ciência e Tecnologia (SFRH/BD/70533/2010 to Inês P. Perpétuo) and by a research grant from Investigator-Initiated Studies Program of Merck Sharp & Dohme Corp. (Merck_P08574 to João E. Fonseca).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationBiomed Res Int. 2017;2017:2690402pt_PT
dc.identifier.doi10.1155/2017/2690402pt_PT
dc.identifier.eissn2314-6141
dc.identifier.issn2314-6133
dc.identifier.urihttp://hdl.handle.net/10451/51417
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherHindawipt_PT
dc.relation.publisherversionhttps://www.hindawi.com/journals/bmri/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleEffect of tumor necrosis factor inhibitor therapy on osteoclasts precursors in rheumatoid arthritispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F70533%2F2010/PT
oaire.citation.endPage10pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleBioMed Research Internationalpt_PT
oaire.citation.volume2017pt_PT
oaire.fundingStreamSFRH
person.familyNamePerpétuo
person.familyNameCaetano-Lopes
person.familyNameRodrigues
person.familyNameCampanilho-Marques
person.familyNamePonte
person.familyNameCanhao
person.familyNameFonseca
person.givenNameInês
person.givenNameJoana
person.givenNameAna Maria
person.givenNameRaquel
person.givenNameCristina
person.givenNameHelena
person.givenNameJoão
person.identifier386523
person.identifier405554
person.identifier.ciencia-idAE18-DA10-460C
person.identifier.ciencia-idFB1D-B9BA-5204
person.identifier.ciencia-id3713-901B-4493
person.identifier.ciencia-idF310-B85D-57C7
person.identifier.orcid0000-0001-7671-2539
person.identifier.orcid0000-0003-0310-4641
person.identifier.orcid0000-0003-2046-8017
person.identifier.orcid0000-0002-1894-8516
person.identifier.orcid0000-0002-3989-1192
person.identifier.orcid0000-0002-3239-2809
person.identifier.orcid0000-0003-1432-3671
person.identifier.ridF-3643-2011
person.identifier.scopus-author-id16300521000
person.identifier.scopus-author-id57189499663
person.identifier.scopus-author-id6602393492
person.identifier.scopus-author-id7101983519
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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