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PLoS One. 2014 Mar 17;9(3):e91996. doi: 10.1371/journal.pone.0091996. eCollection 2014.

Gene silencing of SOCS3 by siRNA intranasal delivery inhibits asthma phenotype in mice.

Author information

1
Department of Immunology, IIS-Fundación Jiménez Díaz, Madrid, Spain; CIBER de Enfermedades Respiratorias, Madrid, Spain.
2
Department of Immunology, IIS-Fundación Jiménez Díaz, Madrid, Spain.
3
CIBER de Enfermedades Respiratorias, Madrid, Spain; Advanced Imaging Unit, Centro Nacional de Investigaciones Cardiovasculares, and Universidad Complutense Madrid, Madrid, Spain.
4
Allergy Section and Experimental Medicine Unit, Gregorio Marañón Hospital, Madrid, Spain.

Erratum in

  • PLoS One. 2014;9(8):e105924.

Abstract

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.

PMID:
24637581
PMCID:
PMC3956882
DOI:
10.1371/journal.pone.0091996
[Indexed for MEDLINE]
Free PMC Article

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