Angiotensin-(1-7) and Alamandine Promote Anti-inflammatory Response in Macrophages In Vitro and In Vivo

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dc.creatorMelissa de Carvalho Santuchi
dc.creatorRicardo Gonçalves
dc.creatorMauro Martins Teixeira
dc.creatorLirlândia Pires Sousa
dc.creatorRobson Augusto Souza Dos Santos
dc.creatorRafaela Fernandes da Silva
dc.creatorMiriane Fernandes Dutra
dc.creatorJuliana Priscila Vago
dc.creatorKátia Maciel Lima
dc.creatorIzabela Galvão
dc.creatorFernando Pedro de Souza-neto
dc.creatorMario Morais e Silva
dc.creatorAline Cristina Oliveira
dc.creatorFlávia Carvalho Bittencourt de Oliveira
dc.date.accessioned2023-09-14T00:31:09Z
dc.date.accessioned2025-09-08T23:37:34Z
dc.date.available2023-09-14T00:31:09Z
dc.date.issued2019-02-21
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1155/2019/2401081
dc.identifier.issn1466-1861
dc.identifier.urihttps://hdl.handle.net/1843/58652
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofMediators of Inflammation
dc.rightsAcesso Aberto
dc.subjectInfeccções
dc.subjectMacrófagos
dc.subject.otherMacrófagos
dc.subject.otherInfeccções
dc.titleAngiotensin-(1-7) and Alamandine Promote Anti-inflammatory Response in Macrophages In Vitro and In Vivo
dc.typeArtigo de periódico
local.citation.epage14
local.citation.spage2401081
local.citation.volume2019
local.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.
local.identifier.orcidhttp://orcid.org/0000-0002-3461-3716
local.identifier.orcidhttp://orcid.org/0000-0001-8188-3738
local.identifier.orcidhttp://orcid.org/0000-0002-6944-3008
local.identifier.orcidhttp://orcid.org/0000-0002-1042-9762
local.identifier.orcidhttp://orcid.org/0000-0001-8738-5852
local.identifier.orcidhttp://orcid.org/0000-0002-3335-2542
local.identifier.orcidhttps://orcid.org/0000-0002-1127-4483
local.publisher.countryBrasil
local.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICAS
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA
local.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.hindawi.com/journals/mi/2019/2401081/#copyright

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