Literature DB >> 28539224

Inhaled ENaC antisense oligonucleotide ameliorates cystic fibrosis-like lung disease in mice.

Jeff R Crosby1, Chenguang Zhao2, Chong Jiang3, Dong Bai2, Melanie Katz2, Sarah Greenlee2, Hiroshi Kawabe4, Michael McCaleb2, Daniela Rotin3, Shuling Guo2, Brett P Monia2.   

Abstract

BACKGROUND: Epithelial sodium channel (ENaC, Scnn1) hyperactivity in the lung leads to airway surface dehydration and mucus accumulation in cystic fibrosis (CF) patients and in mice with CF-like lung disease.
METHODS: We identified several potent ENaC specific antisense oligonucleotides (ASOs) and tested them by inhalation in mouse models of CF-like lung disease.
RESULTS: The inhaled ASOs distributed into lung airway epithelial cells and decreased ENaC expression by inducing RNase H1-dependent degradation of the targeted Scnn1a mRNA. Aerosol delivered ENaC ASO down-regulated mucus marker expression and ameliorated goblet cell metaplasia, inflammation, and airway hyper-responsiveness. Lack of systemic activity of ASOs delivered via the aerosol route ensures the safety of this approach.
CONCLUSIONS: Our results demonstrate that antisense inhibition of ENaC in airway epithelial cells could be an effective and safe approach for the prevention and reversal of lung symptoms in CF and potentially other inflammatory diseases of the lung.
Copyright © 2017 European Cystic Fibrosis Society. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Aerosol; Antisense oligonucleotide; Cystic fibrosis; ENaC

Mesh:

Substances:

Year:  2017        PMID: 28539224     DOI: 10.1016/j.jcf.2017.05.003

Source DB:  PubMed          Journal:  J Cyst Fibros        ISSN: 1569-1993            Impact factor:   5.482


  29 in total

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