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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/58652
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dc.creatorMelissa de Carvalho Santuchipt_BR
dc.creatorRicardo Gonçalvespt_BR
dc.creatorMauro Martins Teixeirapt_BR
dc.creatorLirlândia Pires Sousapt_BR
dc.creatorRobson Augusto Souza Dos Santospt_BR
dc.creatorRafaela Fernandes da Silvapt_BR
dc.creatorMiriane Fernandes Dutrapt_BR
dc.creatorJuliana Priscila Vagopt_BR
dc.creatorKátia Maciel Limapt_BR
dc.creatorIzabela Galvãopt_BR
dc.creatorFernando Pedro de Souza-netopt_BR
dc.creatorMario Morais e Silvapt_BR
dc.creatorAline Cristina Oliveirapt_BR
dc.creatorFlávia Carvalho Bittencourt de Oliveirapt_BR
dc.date.accessioned2023-09-14T00:31:09Z-
dc.date.available2023-09-14T00:31:09Z-
dc.date.issued2019-02-21-
dc.citation.volume2019pt_BR
dc.citation.spage2401081pt_BR
dc.citation.epage14pt_BR
dc.identifier.doihttps://doi.org/10.1155/2019/2401081pt_BR
dc.identifier.issn1466-1861pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/58652-
dc.description.resumoThe renin-angiotensin system (RAS) peptides play an important role in inflammation. Resolution of inflammation contributes to restore tissue homeostasis, and it is characterized by neutrophil apoptosis and their subsequent removal by macrophages, which are remarkable plastic cells involved in the pathophysiology of diverse inflammatory diseases. However, the effects of RAS peptides on different macrophage phenotypes are still emerging. Here, we evaluated the effects of angiotensin-(1-7) (Ang-(1-7)) and the most novel RAS peptide, alamandine, on resting (M0), proinflammatory M(LPS+IFN-γ), and anti-inflammatory M(IL-4) macrophage phenotypes in vitro, as well as on specific immune cell populations and macrophage subsets into the pleural cavity of LPS-induced pleurisy in mice. Our results showed that Ang-(1-7) and alamandine, through Mas and MrgD receptors, respectively, do not affect M0 macrophages but reduce the proinflammatory TNF-α, CCL2, and IL-1β transcript expression levels in LPS+IFN-γ-stimulated macrophages. Therapeutic administration of these peptides in LPS-induced inflammation in mice decreased the number of neutrophils and M1 (F4/80lowGr1+CD11bmed) macrophage frequency without affecting the other investigated macrophage subsets. Our data suggested that both Ang-(1-7) and alamandine, through their respective receptors Mas and MrgD, promote an anti-inflammatory reprogramming of M(LPS+IFN-γ)/M1 macrophages under inflammatory circumstances and potentiate the reprogramming induced by IL-4. In conclusion, our work sheds light on the emerging proresolving properties of Ang-(1-7) and alamandine, opening new avenues for the treatment of inflammatory diseases.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICASpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofMediators of Inflammationpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectMacrófagospt_BR
dc.subjectInfeccçõespt_BR
dc.subject.otherInfeccçõespt_BR
dc.subject.otherMacrófagospt_BR
dc.titleAngiotensin-(1-7) and Alamandine Promote Anti-inflammatory Response in Macrophages In Vitro and In Vivopt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.hindawi.com/journals/mi/2019/2401081/#copyrightpt_BR
dc.identifier.orcidhttp://orcid.org/0000-0002-3461-3716pt_BR
dc.identifier.orcidhttp://orcid.org/0000-0001-8188-3738pt_BR
dc.identifier.orcidhttp://orcid.org/0000-0002-6944-3008pt_BR
dc.identifier.orcidhttp://orcid.org/0000-0002-1042-9762pt_BR
dc.identifier.orcidhttp://orcid.org/0000-0001-8738-5852pt_BR
dc.identifier.orcidhttp://orcid.org/0000-0002-3335-2542pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1127-4483pt_BR
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