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Citations to this article

CFTR and differentiation markers expression in non-CF and delta F 508 homozygous CF nasal epithelium.
F Dupuit, … , B Tümmler, E Puchelle
F Dupuit, … , B Tümmler, E Puchelle
Published September 1, 1995
Citation Information: J Clin Invest. 1995;96(3):1601-1611. https://doi.org/10.1172/JCI118199.
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Research Article

CFTR and differentiation markers expression in non-CF and delta F 508 homozygous CF nasal epithelium.

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Abstract

Human nasal polyps from non-CF and delta F 508 homozygous CF patients were used to compare the expression of CFTR and markers epithelial differentiation, such as cytokeratins (CK) and desmoplakins (DP), at the transcriptional and translational levels. mRNA expression was assessed by semiquantitative RT/PCR kinetic assays while the expression and distribution of proteins were evaluated by immunofluorescence analysis. In parallel, for each nasal tissue specimen, the importance of surface epithelium remodeling and inflammation was estimated after histological observations. Our results show that the steady-state levels of CFTR, CK13, CK18, CK18, CK14, or DP 1 mRNA transcripts in delta F 508 CF nasal polyps were not significantly different from those of non-CF tissues. A variability in the CFTR mRNA transcript level and in the pattern of CFTR immunolabeling has been observed between the different tissue samples. However, no relationship was found between the level of CFTR mRNA transcripts and the CFTR protein expression and distribution, either in the non-CF or in the CF group. The histological observations of non-CF and CF nasal polyp tissue indicated that the huge variations in the expression and distribution of the CFTR protein were associated with the variations in the degree of surface epithelium remodeling and inflammation in the lamina propria. A surface epithelium, showing a slight basal cell hyperplasia phenotype associated with diffuse inflammation, was mainly characterized by a CFTR protein distribution at the apex of ciliated cells in both non-CF and CF specimens. In contrast, in a remodeled surface epithelium associated with severe inflammation, CFTR protein presented either a diffuse distribution in the cytoplasm of ciliated cells, or was absent. These results suggest that abnormal expression and distribution of the CFTR protein of CF airways is not only caused by CFTR mutations. Airway surface epithelium remodeling and inflammation could play a critical role in the posttranscriptional and/or the posttranslational regulation of the CFTR protein expression in non-CF and CF airways.

Authors

F Dupuit, N Kälin, S Brézillon, J Hinnrasky, B Tümmler, E Puchelle

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Total citations by year

Year: 2023 2021 2020 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 1994 1975 Total
Citations: 1 3 2 1 2 1 1 1 6 1 8 7 4 2 3 3 5 6 1 2 5 9 7 2 6 3 1 1 94
Citation information
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Citations to this article in year 2010 (7)

Title and authors Publication Year
Functional analysis of F508del CFTR in native human colon
A Barneveld, F Stanke, S Tamm, B Siebert, G Brandes, N Derichs, M Ballmann, S Junge, B Tümmler
Biochimica et Biophysica Acta 2010
Cystic fibrosis transmembrane conductance regulator trafficking modulates the barrier function of airway epithelial cell monolayers
P LeSimple, J Liao, R Robert, DC Gruenert, JW Hanrahan
The Journal of Physiology 2010
Alternative splicing at a NAGNAG acceptor site as a novel phenotype modifier
A Hinzpeter, A Aissat, E Sondo, C Costa, N Arous, C Gameiro, N Martin, A Tarze, L Weiss, A Becdelièvre, B Costes, M Goossens, LJ Galietta, E Girodon, P Fanen
PLoS genetics 2010
Tissue and Cellular Expression Patterns of Porcine CFTR: Similarities to and Differences From Human CFTR
S Plog, L Mundhenk, MK Bothe, N Klymiuk, AD Gruber
Journal of Histochemistry & Cytochemistry 2010
Long acting β2-agonist and corticosteroid restore airway glandular cell function altered by bacterial supernatant
JM Zahm, F Delavoie, F Toumi, B Nawrocki-Raby, C Kileztky, J Michel, G Balossier, M Johnson, C Coraux, P Birembaut
Respiratory Research 2010
Alternative Splicing at a NAGNAG Acceptor Site as a Novel Phenotype Modifier
A Hinzpeter, A Aissat, E Sondo, C Costa, N Arous, C Gameiro, N Martin, A Tarze, L Weiss, A Becdelièvre, B Costes, M Goossens, LJ Galietta, E Girodon, P Fanen, CE Pearson
PLoS genetics 2010
Nasal Polyposis
TM Önerci, BJ Ferguson
2010

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