2026-04-29T04:09:10Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/73202024-09-27T10:14:12Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19607
Repisalud
author
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
funder
Centro de Investigación Biomedica en Red - CIBER
funder
Instituto de Salud Carlos III
funder
Fundación Conchita Rábago de Jiménez Díaz
2019-03-11T14:35:30Z
2019-03-11T14:35:30Z
2014
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
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.
eng
Gene silencing of SOCS3 by siRNA intranasal delivery inhibits asthma phenotype in mice
journal article
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GeneSilencingSOCS3siRNA_2014.pdf.txt