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dc.contributor.authorZafra, Ma Paz
dc.contributor.authorMazzeo, Carla
dc.contributor.authorGámez, Cristina
dc.contributor.authorRodriguez Marco, Ainara
dc.contributor.authorde Zulueta, Ana
dc.contributor.authorSanz, Veronica
dc.contributor.authorBilbao, Izaskun 
dc.contributor.authorRuiz-Cabello, Jesus 
dc.contributor.authorZubeldia, Jose M
dc.contributor.authordel Pozo, Victoria
dc.date.accessioned2019-03-11T14:35:30Z
dc.date.available2019-03-11T14:35:30Z
dc.date.issued2014
dc.identifier.citationPLoS One. 2014; 9(3):e91996es_ES
dc.identifier.issn1932-6203es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7320
dc.description.abstractSuppresors of cytokine signaling (SOCS) proteins regulate cytokine responses and control immune balance. Several studies have confirmed that SOCS3 is increased in asthmatic patients, and SOCS3 expression is correlated with disease severity. The objective of this study was to evaluate if delivering of SOCS3 short interfering RNA (siRNA) intranasally in lungs could be a good therapeutic approach in an asthma chronic mouse model. Our results showed that intranasal treatment with SOCS3-siRNA led to an improvement in the eosinophil count and the normalization of hyperresponsiveness to methacholine. Concomitantly, this treatment resulted in an improvement in mucus secretion, a reduction in lung collagen, which are prominent features of airway remodeling. The mechanism implies JAK/STAT and RhoA/Rho-kinase signaling pathway, because we found a decreasing in STAT3 phosphorylation status and down regulation of RhoA/Rho-kinase protein expression. These results might lead to a new therapy for the treatment of chronic asthma.es_ES
dc.description.sponsorshipThis study was supported by grants PS09/00153 and PI12/00691 and CIBER de Enfermedades Respiratorias; from Spain’s Health Research Fund, a Carlos III Institute of Health initiative; and fellowship grants from the Conchita Rabago Foundation (PZ).es_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Sciencees_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshAnimals es_ES
dc.subject.meshAsthma es_ES
dc.subject.meshCollagen es_ES
dc.subject.meshCytokines es_ES
dc.subject.meshDisease Models, Animales_ES
dc.subject.meshGene Expression Profiling es_ES
dc.subject.meshGene Expression Regulation es_ES
dc.subject.meshGene Knockdown Techniques es_ES
dc.subject.meshGene Transfer Techniques es_ES
dc.subject.meshImmunity, Humoral es_ES
dc.subject.meshLung es_ES
dc.subject.meshMale es_ES
dc.subject.meshMice es_ES
dc.subject.meshMicroRNAs es_ES
dc.subject.meshPhenotype es_ES
dc.subject.meshRNA, Small Interfering es_ES
dc.subject.meshRespiratory Mucosa es_ES
dc.subject.meshSignal Transduction es_ES
dc.subject.meshSuppressor of Cytokine Signaling 3 Protein es_ES
dc.subject.meshSuppressor of Cytokine Signaling Proteins es_ES
dc.subject.meshX-Ray Microtomography es_ES
dc.subject.meshGene Silencing es_ES
dc.titleGene silencing of SOCS3 by siRNA intranasal delivery inhibits asthma phenotype in micees_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID24637581es_ES
dc.format.volume9es_ES
dc.format.number3es_ES
dc.format.pagee91996es_ES
dc.identifier.doi10.1371/journal.pone.0091996es_ES
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBERes_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderFundación Conchita Rabagoes_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn1932-6203es_ES
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pone.0091996es_ES
dc.identifier.journalPloS onees_ES
dc.repisalud.orgCNICCNIC::Unidades técnicases_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PS09/00153es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI12/00691es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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