2026-04-29T04:10:03Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/73202024-09-27T10:14:12Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19607

00925njm 22002777a 4500 dc Zafra, Ma Paz author Mazzeo, Carla author Gámez, Cristina author Rodriguez Marco, Ainara author de Zulueta, Ana author Sanz, Veronica author Bilbao, Izaskun author Ruiz-Cabello, Jesus author Zubeldia, Jose M author del Pozo, Victoria author 2014 Suppresors 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. PLoS One. 2014; 9(3):e91996 1932-6203 http://hdl.handle.net/20.500.12105/7320 24637581 10.1371/journal.pone.0091996 1932-6203 PloS one Gene silencing of SOCS3 by siRNA intranasal delivery inhibits asthma phenotype in mice