Evidence map›Paper›PMID 33045470›Full record

ArticleEBioMedicine2020

Canonical WNT pathway is activated in the airway epithelium in chronic obstructive pulmonary disease.

François M Carlier, Sébastien Dupasquier, Jérôme Ambroise, Bruno Detry, Marylène Lecocq, Charline Biétry-Claudet, Yassine Boukala, Jean-Luc Gala, Caroline Bouzin, Stijn E Verleden and 4 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 68 citations in OpenAlex.

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  11. Acute exposure to electronic cigarette components alters mRNA expression of pre-osteoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  19. Airway ciliated cells in adult lung homeostasis and COPD.European respiratory review : an official journal of the European Respiratory Society · 2023
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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

14 authors at 4 institutions in 1 country.

François M CarlierPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium; Department of Pneumology, CHU Mont-Godinne UCL Namur, Yvoir, Belgium.
Sébastien DupasquierPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Jérôme AmbroiseCentre de Technologies Moléculaires Appliquées, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Bruno DetryPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Marylène LecocqPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Charline Biétry-ClaudetPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Yassine BoukalaPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Jean-Luc GalaCentre de Technologies Moléculaires Appliquées, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Caroline BouzinIREC Imaging Platform, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Stijn E VerledenLung Transplant Unit, Division of Respiratory Disease, Department of Clinical and Experimental Medicine, Katholieke Universiteit Leuven, Leuven, Belgium.
Delphine HotonDepartment of Clinical Laboratory, Cliniques Universitaires Saint-Luc, Brussels, Belgium.
Sophie GohyPole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium; Department of Pneumology, Cliniques Universitaires Saint-Luc, Brussels, Belgium.
Bertrand BearzattoCentre de Technologies Moléculaires Appliquées, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Charles PilettePole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium; Department of Pneumology, Cliniques Universitaires Saint-Luc, Brussels, Belgium. Electronic address: charles.pilette@uclouvain.be.
UCLouvain · BECliniques Universitaires Saint-Luc · BECHU Dinant Godinne UCL Namur · BEKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is a devastating lung disease, mainly due to cigarette smoking, which represents the third cause of mortality worldwide. The mechanisms driving its epithelial salient features remain largely elusive. We aimed to evaluate the activation and the role of the canonical, β-catenin-dependant WNT pathway in the airway epithelium from COPD patients.

methodsThe WNT/β-catenin pathway was first assessed by WNT-targeted RNA sequencing of the air/liquid interface-reconstituted bronchial epithelium from COPD and control patients. Airway expression of total and active β-catenin was assessed in lung sections, as well as WNT components in laser-microdissected airway epithelium. Finally, we evaluated the role of WNT at the bronchial epithelial level by modulating the pathway in the reconstituted COPD epithelium.

findingsWe show that the WNT/β-catenin pathway is upregulated in the COPD airway epithelium as compared with that of non-smokers and control smokers, in targeted RNA-sequencing of in vitro reconstituted airway epithelium, and in situ in lung tissue and laser-microdissected epithelium. Extrinsic activation of this pathway in COPD-derived airway epithelium inhibited epithelial differentiation, polarity and barrier function, and induced TGF-β-related epithelial-to-mesenchymal transition (EMT). Conversely, canonical WNT inhibition increased ciliated cell numbers, epithelial polarity and barrier function, whilst inhibiting EMT, thus reversing COPD features.

interpretationIn conclusion, the aberrant reactivation of the canonical WNT pathway in the adult airway epithelium recapitulates the diseased phenotype observed in COPD patients, suggesting that this pathway or its downstream effectors could represent a future therapeutic target.

fundingThis study was supported by the Fondation Mont-Godinne, the FNRS and the WELBIO.

Indexed as

Wnt Signaling PathwayAdultAgedbeta CateninBiomarkersCase-Control StudiesCell DifferentiationCells, CulturedDisease SusceptibilityEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene Expression RegulationHumansMalebeta CateninBiomarkersWnt ProteinsAirway epitheliumBarrier dysfunctionCOPDWNTβ-catenin

Identifiers

PMID33045470
PMCPMC7559244
OpenAlexW3092153780

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.