Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/82039
Tipo: Artigo de Periódico
Título: Cigarette smoke induces miR-132 in Th17 cells that enhance osteoclastogenesis in inflammatory arthritis
Autor(es): Paula Barbim Donate
Rene D. Oliveira
Geraldo Aleixo Passos
José Carlos Alves-Filho
Thiago Mattar. Cunha
Paulo Louzada-Junior
Foo Yew Liew
Fernando de Queiroz Cunha
Kalil Alves de Lima
Raphael Sanches Peres
Fausto Almeida
Sandra Yasuyo Fukada Alves
Tarcília Aparecida da Silva
Daniele Carvalho Bernardo Nascimento
Nerry Tatiana Cecilio
Jhimmy Talbot
Resumen: Rheumatoid 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.
Asunto: Th17 cells
Exosomes
Osteogenesis
Arthritis, rheumatoid
Cyclooxygenase 2
Osteoclasts
Tobacco use disorder
Idioma: eng
País: Brasil
Editor: Universidade Federal de Minas Gerais
Sigla da Institución: UFMG
Departamento: FAO - DEPARTAMENTO DE CLÍNICA
Tipo de acceso: Acesso Aberto
Identificador DOI: https://doi.org/10.1073/pnas.2017120118
URI: http://hdl.handle.net/1843/82039
Fecha del documento: 28-dic-2020
metadata.dc.url.externa: https://www.pnas.org/doi/10.1073/pnas.2017120118?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
metadata.dc.relation.ispartof: Proceedings of the National Academy of Sciences of the United States of America
Aparece en las colecciones:Artigo de Periódico

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