Annexin A1 Regulates NLRP3 Inflammasome Activation and Modifies Lipid Release Profile in Isolated Peritoneal Macrophages

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dc.contributor.authorSanches, Jose Marcos
dc.contributor.authorBranco, Laura Migliari
dc.contributor.authorBueno Duarte, Gustavo Henrique
dc.contributor.authorOliani, Sonia Maria [UNESP]
dc.contributor.authorBortoluci, Karina Ramalho
dc.contributor.authorMoreira, Vanessa
dc.contributor.authorGil, Cristiane Damas [UNESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Oeste Paulista
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2020-12-11T19:10:17Z
dc.date.available2020-12-11T19:10:17Z
dc.date.issued2020-04-01
dc.description.abstractAnnexin A1 (AnxA1) is a potent anti-inflammatory protein that downregulates proinflammatory cytokine release. This study evaluated the role of AnxA1 in the regulation of NLRP3 inflammasome activation and lipid release by starch-elicited murine peritoneal macrophages. C57bl/6 wild-type (WT) and AnxA1-null (AnxA1(-/-)) mice received an intraperitoneal injection of 1.5% starch solution for macrophage recruitment. NLRP3 was activated by priming cells with lipopolysaccharide for 3 h, followed by nigericin (1 h) or ATP (30 min) incubation. As expected, nigericin and ATP administration decreased elicited peritoneal macrophage viability and induced IL-1 beta release, more pronounced in the AnxA1(-/-) cells than in the control peritoneal macrophages. In addition, nigericin-activated AnxA1(-/-) macrophages showed increased levels of NLRP3, while points of co-localization of the AnxA1 protein and NLRP3 inflammasome were detected in WT cells, as demonstrated by ultrastructural analysis. The lipidomic analysis showed a pronounced release of prostaglandins in nigericin-stimulated WT peritoneal macrophages, while ceramides were detected in AnxA1(-/-) cell supernatants. Different eicosanoid profiles were detected for both genotypes, and our results suggest that endogenous AnxA1 regulates the NLRP3-derived IL-1 beta and lipid mediator release in macrophages.en
dc.description.affiliationUniv Fed Sao Paulo, Dept Morfol & Genet, BR-04023900 Sao Paulo, Brazil
dc.description.affiliationUniv Oeste Paulista, Fac Med, BR-11410980 Guaruja, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Ciencias Biol, BR-04044010 Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Ctr Terapia Celular & Mol, BR-04044010 Sao Paulo, Brazil
dc.description.affiliationUniv Estadual Campinas, Inst Quim, BR-13083862 Campinas, SP, Brazil
dc.description.affiliationUniv Estadual Paulista, Programa Posgrad Biociencias, Inst Biociencias Letras & Ciencias Exatas IBILCE, BR-15054000 Sao Jose Do Rio Preto, SP, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Farmacol, BR-04044020 Sao Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Programa Posgrad Biociencias, Inst Biociencias Letras & Ciencias Exatas IBILCE, BR-15054000 Sao Jose Do Rio Preto, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipIdFAPESP: 2016/02012-4
dc.description.sponsorshipIdFAPESP: 2017/26872-5
dc.description.sponsorshipIdCAPES: 001
dc.format.extent15
dc.identifierhttp://dx.doi.org/10.3390/cells9040926
dc.identifier.citationCells. Basel: Mdpi, v. 9, n. 4, 15 p., 2020.
dc.identifier.doi10.3390/cells9040926
dc.identifier.urihttp://hdl.handle.net/11449/197794
dc.identifier.wosWOS:000535559500137
dc.language.isoeng
dc.publisherMdpi
dc.relation.ispartofCells
dc.sourceWeb of Science
dc.subjectinflammation
dc.subjectnigericin
dc.subjectpyroptosis
dc.subjectmass spectrometry
dc.subjectlipidomics
dc.titleAnnexin A1 Regulates NLRP3 Inflammasome Activation and Modifies Lipid Release Profile in Isolated Peritoneal Macrophagesen
dc.typeArtigo
dcterms.rightsHolderMdpi
unesp.author.orcid0000-0003-0918-2130[4]
unesp.author.orcid0000-0001-5579-3069[6]
unesp.author.orcid0000-0001-6979-4126[7]

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