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

Overview of attention for article published in Pflügers Archiv - European Journal of Physiology, June 2018
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Title
Expression and function of Anoctamin 1/TMEM16A calcium-activated chloride channels in airways of in vivo mouse models for cystic fibrosis research
Published in
Pflügers Archiv - European Journal of Physiology, June 2018
DOI 10.1007/s00424-018-2160-x
Pubmed ID
Authors

Anne Hahn, Johanna J. Salomon, Dominik Leitz, Dennis Feigenbutz, Lisa Korsch, Ina Lisewski, Katrin Schrimpf, Pamela Millar-Büchner, Marcus A. Mall, Stephan Frings, Frank Möhrlen

Abstract

Physiological processes of vital importance are often safeguarded by compensatory systems that substitute for primary processes in case these are damaged by gene mutation. Ca2+-dependent Cl- secretion in airway epithelial cells may provide such a compensatory mechanism for impaired Cl- secretion via cystic fibrosis transmembrane conductance regulator (CFTR) channels in cystic fibrosis (CF). Anoctamin 1 (ANO1) Ca2+-gated Cl- channels are known to contribute to calcium-dependent Cl- secretion in tracheal and bronchial epithelia. In the present study, two mouse models of CF were examined to assess a potential protective function of Ca2+-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 analyzed. Moreover, Ussing chamber experiments were conducted to compare Ca2+-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 of mouse tracheal and bronchial epithelia. Ciliated cells did not express these proteins. Despite co-localization of CFTR and ANO1 in the same cell type, cells in cftr-/- mice displayed no altered expression of ANO1. Similarly, ANO1 expression was unaffected by βENaC overexpression in the Scnn1b-Tg line. These results suggest that the CF-related environment in the two mouse models did not induce ANO1 overexpression as a compensatory system.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 26 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 19%
Student > Bachelor 3 12%
Researcher 2 8%
Student > Master 2 8%
Student > Doctoral Student 1 4%
Other 3 12%
Unknown 10 38%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 27%
Pharmacology, Toxicology and Pharmaceutical Science 2 8%
Agricultural and Biological Sciences 2 8%
Medicine and Dentistry 2 8%
Sports and Recreations 1 4%
Other 1 4%
Unknown 11 42%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 June 2018.
All research outputs
#16,049,105
of 23,818,521 outputs
Outputs from Pflügers Archiv - European Journal of Physiology
#1,378
of 1,973 outputs
Outputs of similar age
#212,117
of 331,349 outputs
Outputs of similar age from Pflügers Archiv - European Journal of Physiology
#6
of 25 outputs
Altmetric has tracked 23,818,521 research outputs across all sources so far. This one is in the 22nd percentile – i.e., 22% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,973 research outputs from this source. They receive a mean Attention Score of 5.0. This one is in the 23rd percentile – i.e., 23% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 331,349 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 25 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 60% of its contemporaries.