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dc.contributor.authorVilla-Bellosta, Ricardo 
dc.contributor.authorHamczyk, Magda R. 
dc.contributor.authorAndres, Vicente 
dc.date.accessioned2017-10-20T10:33:49Z
dc.date.available2017-10-20T10:33:49Z
dc.date.issued2017
dc.identifierISI:000399175000058
dc.identifier.citationPLoS One. 2017; 12(3):e0174998
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5158
dc.description.abstractPurpose Phosphorus is an essential nutrient involved in many pathobiological processes. Less than 1\% of phosphorus is found in extracellular fluids as inorganic phosphate ion (Pi) in solution. High serum Pi level promotes ectopic calcification in many tissues, including blood vessels. Here, we studied the effect of elevated Pi concentration on macrophage polarization and calcification. Macrophages, present in virtually all tissues, play key roles in health and disease and display remarkable plasticity, being able to change their physiology in response to environmental cues. Methods and results High-throughput transcriptomic analysis and functional studies demonstrated that Pi induces unpolarized macrophages to adopt a phenotype closely resembling that of alternatively -activated M2 macrophages, as revealed by arginine hydrolysis and energetic and antioxidant profiles. Pi-induced macrophages showed an anti-calcifying action mediated by increased availability of extracellular ATP and pyrophosphate. Conclusion We conclude that the ability of Pi-activated macrophages to prevent calcium-phosphate deposition is a compensatory mechanism protecting tissues from hyperphosphatemiainduced pathologic calcification.
dc.description.sponsorshipThe Spanish Ministerio de Economia y Competitividad (MINECO) supports R.V.-B. (Juan de la Cierva JCI-2011-09663 and SAF-201460699-JIN postdoctoral contracts) and M.R.H. (FPI predoctoral contract BES-2011-043938). This study was supported by research grants to V.A. from MINECO (SAF2013-4663-R) and the Institute de Salud Carlos III (RD12/0042/0028) with co-funding from the Fondo Europeo de Desarrollo Regional (FEDER). The CNIC is supported by the MINECO and the Pro-CNIC Foundation, and is a Severo Ochoa Center of Excellence (MINECO award SEV-2015-0505). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
dc.language.isoeng
dc.publisherPublic Library of Science (PLOS) 
dc.type.hasVersionVoR
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectVASCULAR SMOOTH-MUSCLE
dc.subjectCHRONIC KIDNEY-DISEASE
dc.subjectIN-VITRO
dc.subjectMEDIATED INFLAMMATION
dc.subjectCELL CALCIFICATION
dc.subjectMETABOLISM
dc.subjectPOLARIZATION
dc.subjectCALCIUM
dc.subjectATHEROSCLEROSIS
dc.subjectHOMEOSTASIS
dc.titleNovel phosphate-activated macrophages prevent ectopic calcification by increasing extracellular ATP and pyrophosphate
dc.typejournal article
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID28362852
dc.format.volume12
dc.identifier.doi10.1371/journal.pone.0174998
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.contributor.funderFundación ProCNIC 
dc.description.peerreviewed
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pone.0174998
dc.identifier.journalPLoS One
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genética
dc.repisalud.institucionCNIC
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF-2014-60699-JINes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2013-4663-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/JCI-2011-09663es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/BES-2011-043938es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0042/0028es_ES
dc.rights.accessRightsopen accesses_ES


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