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Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis

dc.contributor.authorSantarino, Inês B.
dc.contributor.authorViegas, Michelle S.
dc.contributor.authorDomingues, Neuza S.
dc.contributor.authorRibeiro, Ana M.
dc.contributor.authorSoares, Miguel P.
dc.contributor.authorVieira, Otília V.
dc.date.accessioned2017-07-25T14:38:55Z
dc.date.available2017-07-25T14:38:55Z
dc.date.issued2017-07-19
dc.descriptionThis deposit is composed by the main article plus the supplementary materials of the publication.pt_PT
dc.description.abstractErythrophagocytosis, the phagocytic removal of damaged red blood cells (RBC), and subsequent phagolysosome biogenesis are important processes in iron/heme metabolism and homeostasis. Phagolysosome biogenesis implies the interaction of nascent phagosomes with endocytic compartments and also autophagy effectors. Here, we report that besides recruitment of microtubule-associated protein-1-light chain 3 (LC3), additional autophagy machinery such as sequestosome 1 (p62) is also acquired by single-membrane phagosomes at very early stages of the phagocytic process and that its acquisition is very important to the outcome of the process. In bone marrow-derived macrophages (BMDM) silenced for p62, RBC degradation is inhibited. P62, is also required for nuclear translocation and activation of the transcription factor Nuclear factor E2-related Factor 2 (NRF2) during erythrophagocytosis. Deletion of the Nrf2 allele reduces p62 expression and compromises RBC degradation. In conclusion, we reveal that erythrophagocytosis relies on an interplay between p62 and NRF2, potentially acting as protective mechanism to maintain reactive oxygen species at basal levels and preserve macrophage homeostasis.pt_PT
dc.description.sponsorshipFundação para a Ciência e a Tecnologia grants: (HMSP-ICT/0024/2010, UID/Multi/04462/2013, SFRH/BD/62197/2009, SFRH/BD/90258/2012, SFRH /BD/51877/2012, SFRH/BD/52293/2013, PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010 ); European Union FEDER support: (COMPETE, QREN, PT2020 Partnership Agreement), ERC grant: (ERC-2011-AdG 294709-DAMAGECONTROL).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationSantarino, I. B. et al. Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis. Sci Rep 7, 5812 (2017).pt_PT
dc.identifier.doi10.1038/s41598-017-05687-1pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/778
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherNature Publishing Grouppt_PT
dc.relationSFRH/BD/52293/2013pt_PT
dc.relationA New Approach to Fight Tuberculosis
dc.relationHMSP-ICT/0022/2010pt_PT
dc.relationTissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
dc.relation.publisherversionhttps://www.nature.com/articles/s41598-017-05687-1pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectPhagocytosispt_PT
dc.subjectSickle cell diseasept_PT
dc.titleInvolvement of the p62/NRF2 signal transduction pathway on erythrophagocytosispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleA New Approach to Fight Tuberculosis
oaire.awardTitleTissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876-PPCDTI/HMSP-ICT%2F0024%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FMulti%2F04462%2F2013/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F62197%2F2009/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F90258%2F2012/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F51877%2F2012/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-TOX%2F116627%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/FP7/294709/EU
oaire.citation.endPage16pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleScientific Reportspt_PT
oaire.citation.volume7pt_PT
oaire.fundingStream5876-PPCDTI
oaire.fundingStream5876
oaire.fundingStreamSFRH
oaire.fundingStreamSFRH
oaire.fundingStreamSFRH
oaire.fundingStream3599-PPCDT
oaire.fundingStreamFP7
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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relation.isProjectOfPublication8dd6992e-c7c5-4d81-a9ed-a986b03321d8
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relation.isProjectOfPublication.latestForDiscoveryd792ce20-89d6-4b84-8a4b-22422e7cd888

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