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

Author

Ma Paz Zafra, Carla Mazzeo, Cristina Gámez, Ainara Rodriguez Marco, Ana de Zulueta, Veronica Sanz, Izaskun Bilbao, Jesús Ruiz-Cabello, Jose M Zubeldia, and Victoria del Pozo

Subjects
Medicine, Science
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.

Published
2014
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2. Gene silencing of SOCS3 by siRNA intranasal delivery inhibits asthma phenotype in mice

Author

Victoria del Pozo, Ana de Zulueta, Veronica Sanz, Cristina Gámez, Ainara Rodriguez Marco, Carla Mazzeo, José Manuel Zubeldia, Maria Paz Zafra, Jesús Ruiz-Cabello, Izaskun Bilbao, Centro de Investigación Biomedica en Red - CIBER, Instituto de Salud Carlos III, and Fundación Conchita Rábago de Jiménez Díaz

Subjects
Male, Small interfering RNA, RHOA, Pulmonology, Physiology, medicine.medical_treatment, lcsh:Medicine, Suppressor of Cytokine Signaling Proteins, Mice, Cell Signaling, Immune Physiology, Molecular Cell Biology, Allergies, Medicine and Health Sciences, SOCS3, RNA, Small Interfering, STAT3, lcsh:Science, Lung, Regulation of gene expression, Multidisciplinary, biology, digestive, oral, and skin physiology, Gene Transfer Techniques, General Medicine, Gene Therapy, Animal Models, medicine.anatomical_structure, Cytokine, Phenotype, Gene Knockdown Techniques, Cytokines, Collagen, General Agricultural and Biological Sciences, Research Article, Signal Transduction, Immunology, Mouse Models, Respiratory Mucosa, Immunological Signaling, Research and Analysis Methods, General Biochemistry, Genetics and Molecular Biology, Model Organisms, medicine, Gene silencing, Animals, Animal Models of Disease, Gene Silencing, Molecular Biology Techniques, Molecular Biology, Gene Expression Profiling, lcsh:R, Biology and Life Sciences, Cell Biology, X-Ray Microtomography, Eosinophil, Molecular Development, Asthma, Immunity, Humoral, Disease Models, Animal, MicroRNAs, Gene Expression Regulation, Suppressor of Cytokine Signaling 3 Protein, biology.protein, lcsh:Q, Clinical Immunology, Developmental Biology
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. This 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). Sí

Published
2014

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