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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/82039
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dc.creatorPaula Barbim Donatept_BR
dc.creatorRene D. Oliveirapt_BR
dc.creatorGeraldo Aleixo Passospt_BR
dc.creatorJosé Carlos Alves-Filhopt_BR
dc.creatorThiago Mattar. Cunhapt_BR
dc.creatorPaulo Louzada-Juniorpt_BR
dc.creatorFoo Yew Liewpt_BR
dc.creatorFernando de Queiroz Cunhapt_BR
dc.creatorKalil Alves de Limapt_BR
dc.creatorRaphael Sanches Perespt_BR
dc.creatorFausto Almeidapt_BR
dc.creatorSandra Yasuyo Fukada Alvespt_BR
dc.creatorTarcília Aparecida da Silvapt_BR
dc.creatorDaniele Carvalho Bernardo Nascimentopt_BR
dc.creatorNerry Tatiana Ceciliopt_BR
dc.creatorJhimmy Talbotpt_BR
dc.date.accessioned2025-05-05T22:14:44Z-
dc.date.available2025-05-05T22:14:44Z-
dc.date.issued2020-12-28-
dc.citation.volume118pt_BR
dc.citation.issue1pt_BR
dc.citation.spagee2017120118pt_BR
dc.citation.epagee2017120125pt_BR
dc.identifier.doihttps://doi.org/10.1073/pnas.2017120118pt_BR
dc.identifier.issn1091-6490pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/82039-
dc.description.resumoRheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint destruction and severe morbidity. Cigarette smoking (CS) can exacerbate the incidence and severity of RA. Although Th17 cells and the Aryl hydrocarbon receptor (AhR) have been implicated, the mechanism by which CS induces RA development remains unclear. Here, using transcriptomic analysis, we show that microRNA-132 is specifically induced in Th17 cells in the presence of either AhR agonist or CS-enriched medium. miRNA-132 thus induced is packaged into extracellular vesicles produced by Th17 and acts as a proinflammatory mediator increasing osteoclastogenesis through the down-regulation of COX2. In vivo, articular knockdown of miR-132 in murine arthritis models reduces the number of osteoclasts in the joints. Clinically, RA patients express higher levels of miR-132 than do healthy individuals. This increase is further elevated by cigarette smoking. Together, these results reveal a hitherto unrecognized mechanism by which CS could exacerbate RA and further advance understanding of the impact of environmental factors on the pathogenesis of chronic inflammatory diseases.pt_BR
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americapt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectTh17pt_BR
dc.subjectCigarette smokept_BR
dc.subjectExosomespt_BR
dc.subjectOsteoclastogenesispt_BR
dc.subjectRheumatoid arthritispt_BR
dc.subject.otherTh17 cellspt_BR
dc.subject.otherExosomespt_BR
dc.subject.otherOsteogenesispt_BR
dc.subject.otherArthritis, rheumatoidpt_BR
dc.subject.otherCyclooxygenase 2pt_BR
dc.subject.otherOsteoclastspt_BR
dc.subject.otherTobacco use disorderpt_BR
dc.titleCigarette smoke induces miR-132 in Th17 cells that enhance osteoclastogenesis in inflammatory arthritispt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.pnas.org/doi/10.1073/pnas.2017120118?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmedpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9918-8714pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4408-140Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-8422-8894pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7855-3700pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2585-3870pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4755-1670pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9149-168Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0417-779Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6589-4784pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9623-7835pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0620-339Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-5465-5238pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0347-5074pt_BR
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