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ATP modulates acute inflammation In Vivo through Dual Oxidase 1–derived H2O2 production and NF-κB activation

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dc.contributor.authorDe Oliveira, Sofia
dc.contributor.authorLópez-Muñoz, Azucena
dc.contributor.authorCandel, Sergio
dc.contributor.authorPelegrín, Pablo
dc.contributor.authorCalado, Ângelo
dc.contributor.authorMulero, Victoriano
dc.date.accessioned2022-02-10T17:15:31Z
dc.date.available2022-02-10T17:15:31Z
dc.date.issued2014
dc.descriptionCopyright © 2014 by The American Association of Immunologists, Inc.pt_PT
dc.description.abstractDual oxidase 1 (Duox1) is the NADPH oxidase responsible for the H2O2 gradient formed in tissues after injury to trigger the early recruitment of leukocytes. Little is known about the signals that modulate H2O2 release from DUOX1 and whether the H2O2 gradient can orchestrate the inflammatory response in vivo. In this study, we report on a dominant-negative form of zebrafish Duox1 that is able to inhibit endogenous Duox1 activity, H2O2 release and leukocyte recruitment after tissue injury, with none of the side effects associated with morpholino-mediated Duox1 knockdown. Using this specific tool, we found that ATP release following tissue injury activates purinergic P2Y receptors, and modulates Duox1 activity through phospholipase C (PLC) and intracellular calcium signaling in vivo. Furthermore, Duox1-derived H2O2 is able to trigger the NF-κB inflammatory signaling pathway. These data reveal that extracellular ATP acting as an early danger signal is responsible for the activation of Duox1 via a P2YR/PLC/Ca(2+) signaling pathway and the production of H2O2, which, in turn, is able to modulate in vivo not only the early recruitment of leukocytes to the wound but also the inflammatory response through activation of the NF-κB signaling pathway.pt_PT
dc.description.sponsorshipThis work was supported by Fundação para a Ciência e Tecnologia Ph.D. Fellowship Grant SFRH/BD/62674/2009 (to S.d.O.) and Spanish Ministry of Economy and Competitiveness Grant BIO2011-23400 (to V.M.), cofunded with Fondos Europeos de Desarrollo Regional/European Regional Development funds. S.C. was a recipient of a Ph.D. fellowship from the Spanish Ministry of Economy and Competitiveness. This work was also funded by Fundación Séneca-Murcia Grant 04538/GERM/06 (to V.M.).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationJ Immunol 2014; 192:5710-5719pt_PT
dc.identifier.doi10.4049/jimmunol.1302902pt_PT
dc.identifier.eissn1550-6606
dc.identifier.issn0022-1767
dc.identifier.urihttp://hdl.handle.net/10451/51218
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherThe American Association of Immunologists, Inc.pt_PT
dc.relationIN VIVO IMAGING OF INFLAMMATION IN ZEBRAFISH: THE ROLE OF CHEMOKINE SYSTEM IN NEUTROPHIL AND MACROPHAGE MIGRATION
dc.relation.publisherversionhttps://www.jimmunol.org/pt_PT
dc.titleATP modulates acute inflammation In Vivo through Dual Oxidase 1–derived H2O2 production and NF-κB activationpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleIN VIVO IMAGING OF INFLAMMATION IN ZEBRAFISH: THE ROLE OF CHEMOKINE SYSTEM IN NEUTROPHIL AND MACROPHAGE MIGRATION
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F62674%2F2009/PT
oaire.citation.endPage5719pt_PT
oaire.citation.issue12pt_PT
oaire.citation.startPage5710pt_PT
oaire.citation.titleThe Journal of Immunologypt_PT
oaire.citation.volume192pt_PT
person.familyNameDe Oliveira
person.familyNameCalado
person.givenNameSofia
person.givenNameÂngelo
person.identifier1026730
person.identifier.ciencia-id7011-768C-81B6
person.identifier.ciencia-id6214-D18D-843F
person.identifier.orcid0000-0003-0893-111X
person.identifier.orcid0000-0003-0182-2615
person.identifier.ridY-2296-2019
person.identifier.scopus-author-id24476411300
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication007f8d3b-8acf-47bd-8eb8-b8f33d6b9d2b
relation.isAuthorOfPublicationab22c763-5ad6-4837-a6db-a959b1dbb675
relation.isAuthorOfPublication.latestForDiscoveryab22c763-5ad6-4837-a6db-a959b1dbb675
relation.isProjectOfPublication66b32d6f-6829-43b7-a33d-4c39801b18a1
relation.isProjectOfPublication.latestForDiscovery66b32d6f-6829-43b7-a33d-4c39801b18a1

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