ArticlePloS one2015
KCa3.1 K+ Channel Expression and Function in Human Bronchial Epithelial Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Airway remodelling rather than cellular infiltration characterizes both type2 cytokine biomarker-high and -low severe asthma.Allergy · 2022Trial
- Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026Review
- Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on ClInternational journal of molecular sciences · 2023Review
- Unraveling the Role of Epithelial Cells in the Development of Chronic Rhinosinusitis.International journal of molecular sciences · 2023Review
- Ion Transport and Radioresistance.Reviews of physiology, biochemistry and pharmacology · 2022Review
- ATP-evoked intracellular CaJournal of neuroinflammation · 2021Article
- CaBritish journal of pharmacology · 2020Review
- Identification of Clotrimazole Derivatives as Specific Inhibitors of Arenavirus Fusion.Journal of virology · 2019Article
- Ion Channels in Brain Metastasis.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The KCa3.1 K+ channel has been proposed as a novel target for pulmonary diseases such as asthma and pulmonary fibrosis. It is expressed in epithelia but its expression and function in primary human bronchial epithelial cells (HBECs) has not been described. Due to its proposed roles in the regulation of cell proliferation, migration, and epithelial fluid secretion, inhibiting this channel might have either beneficial or adverse effects on HBEC function. The aim of this study was to assess whether primary HBECs express the KCa3.1 channel and its role in HBEC function. Primary HBECs from the airways of healthy and asthmatic subjects, SV-transformed BEAS-2B cells and the neoplastic H292 epithelial cell line were studied. Primary HBECs, BEAS-2B and H292 cells expressed KCa3.1 mRNA and protein, and robust KCa3.1 ion currents. KCa3.1 protein expression was increased in asthmatic compared to healthy airway epithelium in situ, and KCa3.1 currents were larger in asthmatic compared to healthy HBECs cultured in vitro. Selective KCa3.1 blockers (TRAM-34, ICA-17043) had no effect on epithelial cell proliferation, wound closure, ciliary beat frequency, or mucus secretion. However, several features of TGFβ1-dependent epithelial-mesenchymal transition (EMT) were inhibited by KCa3.1 blockade. Treatment with KCa3.1 blockers is likely to be safe with respect to airway epithelial biology, and may potentially inhibit airway remodelling through the inhibition of EMT.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.