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dc.contributor.authorUcero, Álvaro C.
dc.contributor.authorBerzal, Sergio
dc.contributor.authorOcaña-Salceda, Carlos
dc.contributor.authorSancho, Mónica
dc.contributor.authorOrzáez, Mar
dc.contributor.authorMesseguer, Ángel
dc.contributor.authorRuíz-Ortega, Marta
dc.contributor.authorEgido, Jesús
dc.contributor.authorVicent, María J.
dc.contributor.authorOrtíz, Alberto
dc.contributor.authorRamos, Adrián M.
dc.contributor.otherUAM. Departamento de Medicinaes_ES
dc.date.accessioned2014-07-02T09:20:40Z
dc.date.available2014-07-02T09:20:40Z
dc.date.issued2013-01-02
dc.identifier.citationPLoS one 8.1 (2013): e51992en_US
dc.identifier.issn1932-6203 (online)es_ES
dc.identifier.urihttp://hdl.handle.net/10486/660684
dc.description.abstractThe polyglutamic acid/peptoid 1 (QM56) nanoconjugate inhibits apoptosis by interfering with Apaf-1 binding to procaspase-9. We now describe anti-inflammatory properties of QM56 in mouse kidney and renal cell models. In cultured murine tubular cells, QM56 inhibited the inflammatory response to Tweak, a non-apoptotic stimulus. Tweak induced MCP-1 and Rantes synthesis through JAK2 kinase and NF-kB activation. Similar to JAK2 kinase inhibitors, QM56 inhibited Tweak-induced NF-kB transcriptional activity and chemokine expression, despite failing to inhibit NF-kB-p65 nuclear translocation and NF-kB DNA binding. QM56 prevented JAK2 activation and NF-kB-p65(Ser536) phosphorylation. The anti-inflammatory effect and JAK2 inhibition by QM56 were observed in Apaf-12/2 cells. In murine acute kidney injury, QM56 decreased tubular cell apoptosis and kidney inflammation as measured by downmodulations of MCP-1 and Rantes mRNA expression, immune cell infiltration and activation of the JAK2-dependent inflammatory pathway. In conclusion, QM56 has an anti-inflammatory activity which is independent from its role as inhibitor of Apaf-1 and apoptosis and may have potential therapeutic relevance.en_US
dc.description.sponsorshipThis work was supported by grants from the Instituto de Salud Carlos III (www.isciii.es), FIS: PI07/0020, CP08/1083, PS09/00447 and ISCIII-RETICS REDINREN RD 06/0016; Sociedad Española de Nefrología (www.senefro.org). Álvaro Ucero, Sergio Berzal and Carlos Ocaña supported by Fundacion Conchita Rabago (www.fundacionconchitarabago.net), Alberto Ortiz by the Programa de Intensificación de la Actividad Investigadora in the Sistema Nacional de Salud of the Instituto de Salud Carlos III and the Agencia ‘‘Pedro Lain Entralgo’’ of the Comunidad de Madrid and CIFRA S-BIO 0283/2006 www.madrid.org/lainentralgo) and Adrián Ramos, by FIS (Programa Miguel Servet).en_US
dc.format.extent14 pag.es_ES
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Scienceen_US
dc.relation.ispartofPLoS ONEen_US
dc.rights© 2013 Ucero et al.es_ES
dc.subject.otherApoptosisen_US
dc.subject.otherChemokinesen_US
dc.subject.otherCytokinesen_US
dc.subject.otherDNA transcriptionen_US
dc.subject.otherInflammationen_US
dc.subject.otherInflammatory diseasesen_US
dc.subject.otherKidneysen_US
dc.subject.otherPhosphorylationen_US
dc.titleA polymeric nanomedicine diminishes inflammatory events in renal tubular cellsen_US
dc.typearticleen
dc.subject.ecienciaMedicinaes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1371/journal.pone.0051992es_ES
dc.identifier.doi10.1371/journal.pone.0051992es_ES
dc.identifier.publicationfirstpagee51992es_ES
dc.identifier.publicationissue1es_ES
dc.identifier.publicationlastpagee51992es_ES
dc.identifier.publicationvolume8es_ES
dc.relation.projectIDComunidad de Madrid. S2010/BMD-2378/CIFRAes_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersiones_ES
dc.rights.accessRightsopenAccessen
dc.facultadUAMFacultad de Medicina
dc.institutoUAMInstituto de Investigaciones Biomédicas "Alberto Sols" (IIBM)
dc.institutoUAMInstituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD)


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