Expression and function of Anoctamin 1/TMEM16A calcium-activated chloride channels in airways of in vivo mouse models for cystic fibrosis research

Expression and function of Anoctamin 1/TMEM16A calcium-activated chloride channels in airways of... Physiological processes of vital importance are often safeguarded by compensatory systems that substitute for primary 2+ − processes in case these are damaged by gene mutation. Ca -dependent Cl secretion in airway epithelial cells may provide such a compensatory mechanism for impaired Cl secretion via cystic fibrosis transmembrane conductance 2+ − regulator (CFTR) channels in cystic fibrosis (CF). Anoctamin 1 (ANO1) Ca -gated Cl channels are known to con- tribute to calcium-dependent Cl secretion in tracheal and bronchial epithelia. In the present study, two mouse models of 2+ − CF were examined to assess a potential protective function of Ca -dependent Cl secretion, a CFTR deletion model −/− + (cftr ), and a CF pathology model that overexpresses the epithelial Na channel β-subunit (βENaC), which is encoded by the Scnn1b gene, specifically in airway epithelia (Scnn1b-Tg). The expression levels of ANO1 were examined by mRNA and protein content, and the channel protein distribution between ciliated and non-ciliated epithelial cells was 2+ − analyzed. Moreover, Ussing chamber experiments were conducted to compare Ca -dependent Cl secretion between wild-type animals and the two mouse models. Our results demonstrate that CFTR and ANO1 channels were co- expressed with ENaC in non-ciliated cells http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pflügers Archiv European Journal of Physiologyl of Physiology Springer Journals

Expression and function of Anoctamin 1/TMEM16A calcium-activated chloride channels in airways of in vivo mouse models for cystic fibrosis research

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2018 by Springer-Verlag GmbH Germany, part of Springer Nature
Subject
Biomedicine; Human Physiology; Molecular Medicine; Neurosciences; Cell Biology; Receptors
ISSN
0031-6768
eISSN
1432-2013
D.O.I.
10.1007/s00424-018-2160-x
Publisher site
See Article on Publisher Site

Abstract

Physiological processes of vital importance are often safeguarded by compensatory systems that substitute for primary 2+ − processes in case these are damaged by gene mutation. Ca -dependent Cl secretion in airway epithelial cells may provide such a compensatory mechanism for impaired Cl secretion via cystic fibrosis transmembrane conductance 2+ − regulator (CFTR) channels in cystic fibrosis (CF). Anoctamin 1 (ANO1) Ca -gated Cl channels are known to con- tribute to calcium-dependent Cl secretion in tracheal and bronchial epithelia. In the present study, two mouse models of 2+ − CF were examined to assess a potential protective function of Ca -dependent Cl secretion, a CFTR deletion model −/− + (cftr ), and a CF pathology model that overexpresses the epithelial Na channel β-subunit (βENaC), which is encoded by the Scnn1b gene, specifically in airway epithelia (Scnn1b-Tg). The expression levels of ANO1 were examined by mRNA and protein content, and the channel protein distribution between ciliated and non-ciliated epithelial cells was 2+ − analyzed. Moreover, Ussing chamber experiments were conducted to compare Ca -dependent Cl secretion between wild-type animals and the two mouse models. Our results demonstrate that CFTR and ANO1 channels were co- expressed with ENaC in non-ciliated cells

Journal

Pflügers Archiv European Journal of Physiologyl of PhysiologySpringer Journals

Published: Jun 2, 2018

References

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