Zafra, Ma PazMazzeo, CarlaGámez, CristinaRodriguez Marco, Ainarade Zulueta, AnaSanz, VeronicaBilbao, IzaskunRuiz-Cabello, JesusZubeldia, Jose Mdel Pozo, Victoria2019-03-112019-03-112014PLoS One. 2014; 9(3):e919961932-6203http://hdl.handle.net/20.500.12105/7320Suppresors 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.engVoRhttp://creativecommons.org/licenses/by/4.0/AnimalsAsthmaCollagenCytokinesDisease Models, AnimalGene Expression ProfilingGene Expression RegulationGene Knockdown TechniquesGene Transfer TechniquesImmunity, HumoralLungMaleMiceMicroRNAsPhenotypeRNA, Small InterferingRespiratory MucosaSignal TransductionSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsX-Ray MicrotomographyGene SilencingGene silencing of SOCS3 by siRNA intranasal delivery inhibits asthma phenotype in miceAtribución 4.0 Internacional2463758193e9199610.1371/journal.pone.00919961932-6203PloS oneopen access