Evidence map›Paper›PMID 24945658›Full record

ArticlePloS one2014

Paracellular transport through healthy and cystic fibrosis bronchial epithelial cell lines--do we have a proper model?

Natalia Molenda, Katarina Urbanova, Nelly Weiser, Kristina Kusche-Vihrog, Dorothee Günzel, Hermann Schillers

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  14. Junctional abnormalities in human airway epithelial cells expressing F508del CFTR.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  15. Claudins: Gatekeepers of lung epithelial function.Seminars in cell & developmental biology · 2015
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Natalia MolendaInstitute of Physiology II, University of Münster, Münster, Germany.
Katarina UrbanovaInstitute of Physiology II, University of Münster, Münster, Germany.
Nelly WeiserInstitute of Physiology II, University of Münster, Münster, Germany.
Kristina Kusche-VihrogInstitute of Physiology II, University of Münster, Münster, Germany.
Dorothee GünzelInstitute of Clinical Physiology, Charité Campus Benjamin Franklin, Berlin, Germany.
Hermann SchillersInstitute of Physiology II, University of Münster, Münster, Germany.
University of Münster · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been reported recently that the cystic fibrosis transmembrane conductance regulator (CFTR) besides transcellular chloride transport, also controls the paracellular permeability of bronchial epithelium. The aim of this study was to test whether overexpressing wtCFTR solely regulates paracellular permeability of cell monolayers. To answer this question we used a CFBE41o- cell line transfected with wtCFTR or mutant F508del-CFTR and compered them with parental line and healthy 16HBE14o- cells. Transepithelial electrical resistance (TER) and paracellular fluorescein flux were measured under control and CFTR-stimulating conditions. CFTR stimulation significant decreased TER in 16HBE14o- and also in CFBE41o- cells transfected with wtCFTR. In contrast, TER increased upon stimulation in CFBE41o- cells and CFBE41o- cells transfected with F508del-CFTR. Under non-stimulated conditions, all four cell lines had similar paracellular fluorescein flux. Stimulation increased only the paracellular permeability of the 16HBE14o- cell monolayers. We observed that 16HBE14o- cells were significantly smaller and showed a different structure of cell-cell contacts than CFBE41o- and its overexpressing clones. Consequently, 16HBE14o- cells have about 80% more cell-cell contacts through which electrical current and solutes can leak. Also tight junction protein composition is different in 'healthy' 16HBE14o- cells compared to 'cystic fibrosis' CFBE41o- cells. We found that claudin-3 expression was considerably stronger in 16HBE14o- cells than in the three CFBE41o- cell clones and thus independent of the presence of functional CFTR. Together, CFBE41o- cell line transfection with wtCFTR modifies transcellular conductance, but not the paracellular permeability. We conclude that CFTR overexpression is not sufficient to fully reconstitute transport in CF bronchial epithelium. Hence, it is not recommended to use those cell lines to study CFTR-dependent epithelial transport.

Indexed as

Biological TransportBronchiCell LineClaudin-3Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorElectric ImpedanceEpithelial CellsFluoresceinGene ExpressionHumansModels, BiologicalMutationPermeabilityRespiratory MucosaSignal TransductionCFTR protein, humanClaudin-3CLDN3 protein, humanCystic Fibrosis Transmembrane Conductance RegulatorFluorescein

Identifiers

PMID24945658
PMCPMC4063962
OpenAlexW2089102290

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.