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Macrophage and epithelial cell H-ferritin expression regulates renal inflammation

2015-04-15Journal article Open access
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dc.contributor.authorBolisetty, Subhashini
dc.contributor.authorZarjou, Abolfazl
dc.contributor.authorHull, Travis D.
dc.contributor.authorTraylor, Amie M.
dc.contributor.authorPerianayagam, Anjana
dc.contributor.authorJoseph, Reny
dc.contributor.authorKamal, Ahmed I.
dc.contributor.authorArosio, Paolo
dc.contributor.authorSoares, Miguel P.
dc.contributor.authorJeney, Viktoria
dc.contributor.authorBalla, Jozsef
dc.contributor.authorGeorge, James F.
dc.contributor.authorAgarwal, Anupam
dc.date.accessioned2017-06-22T17:39:58Z
dc.date.available2017-06-22T17:39:58Z
dc.date.issued2015-04-15
dc.descriptionThe deposited article is a post-print version (author's manuscript from PMC).pt_PT
dc.descriptionThis publication hasn't any creative commons license associated.pt_PT
dc.descriptionThe deposited article version contains attached the supplementary materials within the pdf.pt_PT
dc.description.abstractInflammation culminating in fibrosis contributes to progressive kidney disease. Cross-talk between the tubular epithelium and interstitial cells regulates inflammation by a coordinated release of cytokines and chemokines. Here we studied the role of heme oxygenase-1 (HO-1) and the heavy subunit of ferritin (FtH) in macrophage polarization and renal inflammation. Deficiency in HO-1 was associated with increased FtH expression, accumulation of macrophages with a dysregulated polarization profile, and increased fibrosis following unilateral ureteral obstruction in mice: a model of renal inflammation and fibrosis. Macrophage polarization in vitro was predominantly dependent on FtH expression in isolated bone marrow-derived mouse monocytes. Using transgenic mice with conditional deletion of FtH in the proximal tubules (FtH(PT-/-)) or myeloid cells (FtH(LysM-/-)), we found that myeloid FtH deficiency did not affect polarization or accumulation of macrophages in the injured kidney compared with wild-type (FtH(+/+)) controls. However, tubular FtH deletion led to a marked increase in proinflammatory macrophages. Furthermore, injured kidneys from FtH(PT-/-) mice expressed significantly higher levels of inflammatory chemokines and fibrosis compared with kidneys from FtH(+/+) and FtH(LysM-/-) mice. Thus, there are differential effects of FtH in macrophages and epithelial cells, which underscore the critical role of FtH in tubular-macrophage cross-talk during kidney injury.pt_PT
dc.description.sponsorshipNIH grants: (R01 DK5960, R01 DK5960, P30 DK079337, R01 DK083390); Fundação para a Ciência e Tecnologia grants: (PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010); European Union grant: (ERC-2011-AdG. 294709 DAMAGECONTROL); AHA grant: (11POST7600074).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationSubhashini Bolisetty, Abolfazl Zarjou, Travis D. Hull, Amie M. Traylor, Anjana Perianayagam, Reny Joseph, Ahmed I. Kamal, Paolo Arosio, Miguel P. Soares, Viktoria Jeney, Jozsef Balla, James F. George, Anupam Agarwal, Macrophage and epithelial cell H-ferritin expression regulates renal inflammation, Kidney International, Volume 88, Issue 1, 2015, Pages 95-108, ISSN 0085-2538, http://dx.doi.org/10.1038/ki.2015.102. (http://www.sciencedirect.com/science/article/pii/S2157171615321183) Keywords: acute kidney injury; ferritin; fibrosis; inflammation; macrophage polarizationpt_PT
dc.identifier.doi10.1038/ki.2015.102pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/770
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relationNIH - P30 AR048311pt_PT
dc.relationNIH - P30 AI027767pt_PT
dc.relationNIH - R01 DK5960pt_PT
dc.relationNIH - P30 DK079337pt_PT
dc.relationNIH - R01 DK083390pt_PT
dc.relationHMSP-ICT/0022/2010pt_PT
dc.relationTissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S2157171615321183?via%3Dihubpt_PT
dc.subjectAnimalspt_PT
dc.subjectApoferritinspt_PT
dc.subjectCells, Culturedpt_PT
dc.subjectChemokine CCL2pt_PT
dc.subjectDisease Models, Animalpt_PT
dc.subjectEpithelial Cellspt_PT
dc.subjectFibrosispt_PT
dc.subjectGene Expressionpt_PT
dc.subjectHeme Oxygenase-1pt_PT
dc.subjectInterleukin-10pt_PT
dc.subjectInterleukin-6pt_PT
dc.subjectKidneypt_PT
dc.subjectKidney Tubules, Proximalpt_PT
dc.subjectMacrophage Activationpt_PT
dc.subjectMacrophage Colony-Stimulating Factorpt_PT
dc.subjectMacrophagespt_PT
dc.subjectMalept_PT
dc.subjectMicept_PT
dc.subjectMice, Inbred C57BLpt_PT
dc.subjectMice, Transgenicpt_PT
dc.subjectMyeloid Cellspt_PT
dc.subjectNephritispt_PT
dc.subjectRNA, Messengerpt_PT
dc.subjectUreteral Obstructionpt_PT
dc.titleMacrophage and epithelial cell H-ferritin expression regulates renal inflammationpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleTissue Damage Control Regulates The Pathogenesis of Immune Mediated Inflammatory Diseases
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.endPage108pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage95pt_PT
oaire.citation.titleKidney Internationalpt_PT
oaire.citation.volume88pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStreamFP7
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.nameEuropean Commission
rcaap.embargofctThis uploaded article had a 24-month embargo period in terms of access, due to the journal's policies and publisher's copyright policy, which require an embargo period between 12 months and 48 months.pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication72d8fa6f-1215-4a61-bc70-515eef334d45
relation.isProjectOfPublication370f9aad-c4ef-4e35-b754-edc840dc6b5e
relation.isProjectOfPublication.latestForDiscovery370f9aad-c4ef-4e35-b754-edc840dc6b5e

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