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Specific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injury

2017-03-15Journal article Open access
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dc.contributor.authorRossi, Maxime
dc.contributor.authorThierry, Antoine
dc.contributor.authorDelbauve, Sandrine
dc.contributor.authorPreyat, Nicolas
dc.contributor.authorSoares, Miguel P.
dc.contributor.authorRoumeguère, Thierry
dc.contributor.authorLeo, Oberdan
dc.contributor.authorFlamand, Véronique
dc.contributor.authorLe Moine, Alain
dc.contributor.authorHougardy, Jean-Michel
dc.date.accessioned2017-03-17T15:25:35Z
dc.date.available2017-03-17T15:25:35Z
dc.date.issued2017-03-15
dc.descriptionThis work was presented in abstract form at the 17th Congress of the European Society for Organ Transplantation (ESOT) in Brussels, Belgium (Brief Oral Presentation, BOS04 – Ischemia, Reperfusion, Metabolism and Aging, abstract N°BO33; 13–16 September 2015) and at the 16th Congress of the European Association of Urology (EAU) in Munich, Germany (Poster Session 48, Kidney Transplant: From Bench to clinical practice, abstract n°603; 11–15 March 2016).pt_PT
dc.description.abstractRenal ischemia-reperfusion injury (IRI) is a major risk factor for delayed graft function in renal transplantation. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1) mediates protection against IRI. However, the role of myeloid HO-1 during IRI remains poorly characterized. Mice with myeloid-restricted deletion of HO-1 (HO-1(M-KO)), littermate (LT), and wild-type (WT) mice were subjected to renal IRI or sham procedures and sacrificed after 24 hours or 7 days. In comparison to LT, HO-1(M-KO) exhibited significant renal histological damage, pro-inflammatory responses and oxidative stress 24 hours after reperfusion. HO-1(M-KO) mice also displayed impaired tubular repair and increased renal fibrosis 7 days after IRI. In WT mice, HO-1 induction with hemin specifically upregulated HO-1 within the CD11b(+) F4/80(lo) subset of the renal myeloid cells. Prior administration of hemin to renal IRI was associated with significant increase of the renal HO-1(+) CD11b(+) F4/80(lo) myeloid cells in comparison to control mice. In contrast, this hemin-mediated protection was abolished in HO-1(M-KO) mice. In conclusion, myeloid HO-1 appears as a critical protective pathway against renal IRI and could be an interesting therapeutic target in renal transplantation.pt_PT
dc.description.sponsorshipFonds de la Recherche Scientifique Médicale; Fonds Erasme pour la Recherche Médicale; Société Belge d’Urologie.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationScientific Reports 7, Article number: 197 (2017) doi:10.1038/s41598-017-00220-wpt_PT
dc.identifier.doi10.1038/s41598-017-00220-wpt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/739
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherNature Publishing Grouppt_PT
dc.relation.publisherversionhttp://www.nature.com/articles/s41598-017-00220-w?WT.feed_name=subjects_immunologypt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAcute kidney injurypt_PT
dc.subjectMonocytes and macrophagespt_PT
dc.subjectTranslational immunologypt_PT
dc.titleSpecific expression of heme oxygenase-1 by myeloid cells modulates renal ischemia-reperfusion injurypt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage14pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleScientific Reportspt_PT
oaire.citation.volume7pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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