Evidence map›Paper›PMID 23431157›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Contribution of α7 nicotinic receptor to airway epithelium dysfunction under nicotine exposure.

Kamel Maouche, Kahina Medjber, Jean-Marie Zahm, Franck Delavoie, Christine Terryn, Christelle Coraux, Stéphanie Pons, Isabelle Cloëz-Tayarani, Uwe Maskos, Philippe Birembaut and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024
    Review
  6. Article
  7. Vaping-Induced Proteolysis Causes Airway Surface Dehydration.International journal of molecular sciences · 2023
    Article
  8. Review
  9. Nicotine aerosols diminish airway CFTR function and mucociliary clearance.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  10. Article
  11. Vaping-Associated Lung Injury: A Review.Medicina (Kaunas, Lithuania) · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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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

11 authors at 3 institutions in 1 country.

Kamel MaoucheInstitut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche-Santé 903, 51092 Reims, France.
Kahina Medjber
Jean-Marie Zahm
Franck Delavoie
Christine Terryn
Christelle Coraux
Stéphanie Pons
Isabelle Cloëz-Tayarani
Uwe Maskos
Philippe Birembaut
Jean-Marie Tournier
Université de Reims Champagne-Ardenne · FRInserm · FRLaboratoire de Neurosciences Cognitives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss or dysfunction of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) leads to impairment of airway mucus transport and to chronic lung diseases resulting in progressive respiratory failure. Nicotinic acetylcholine receptors (nAChRs) bind nicotine and nicotine-derived nitrosamines and thus mediate many of the tobacco-related deleterious effects in the lung. Here we identify α7 nAChR as a key regulator of CFTR in the airways. The airway epithelium in α7 knockout mice is characterized by a higher transepithelial potential difference, an increase of amiloride-sensitive apical Na(+) absorption, a defective cAMP-dependent Cl(-) conductance, higher concentrations of Na(+), Cl(-), K(+), and Ca(2+) in secretions, and a decreased mucus transport, all relevant to a deficient CFTR activity. Moreover, prolonged nicotine exposure mimics the absence of α7 nAChR in mice or its inactivation in vitro in human airway epithelial cell cultures. The functional coupling of α7 nAChR to CFTR occurs through Ca(2+) entry and activation of adenylyl cyclases, protein kinase A, and PKC. α7 nAChR, CFTR, and adenylyl cyclase-1 are physically and functionally associated in a macromolecular complex within lipid rafts at the apical membrane of surface and glandular airway epithelium. This study establishes the potential role of α7 nAChR in the regulation of CFTR function and in the pathogenesis of smoking-related chronic lung diseases.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsBungarotoxinsCalciumCells, CulturedChloridesCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorHumansIon TransportMembrane MicrodomainsMiceMice, Inbred C57BLMice, KnockoutNicotineReceptors, Nicotinicalpha7 Nicotinic Acetylcholine ReceptorBungarotoxinsCalciumCFTR protein, humanChloridesChrna7 protein, humanChrna7 protein, mouseCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorNicotineReceptors, Nicotinic

Identifiers

PMID23431157
PMCPMC3593882
OpenAlexW1968523639

What OpenQuestion holds

Textmetadata
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.