dc.contributor.author
Molenda, Natalia
dc.contributor.author
Urbanova, Katarina
dc.contributor.author
Weiser, Nelly
dc.contributor.author
Kusche-Vihrog, Kristina
dc.contributor.author
Günzel, Dorothee
dc.contributor.author
Schillers, Hermann
dc.date.accessioned
2018-06-08T02:56:41Z
dc.date.available
2014-09-25T18:55:16.761Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/14184
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-18381
dc.description.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.
de
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Paracellular Transport through Healthy and Cystic Fibrosis Bronchial
Epithelial Cell Lines
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
PLoS ONE 9 (2014), 6, Artikel Nr. e100621
dc.title.subtitle
Do We Have a Proper Model?
dcterms.bibliographicCitation.doi
10.1371/journal.pone.0100621
dcterms.bibliographicCitation.url
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0100621
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000021030
refubium.note.author
Der Artikel wurde in einer Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000003962
dcterms.accessRights.openaire
open access