Evidence map›Paper›PMID 16938132›Full record

ArticleRespiratory research2006

Evidence that CFTR is expressed in rat tracheal smooth muscle cells and contributes to bronchodilation.

Clarisse Vandebrouck, Patricia Melin, Caroline Norez, Renaud Robert, Christelle Guibert, Yvette Mettey, Frédéric Becq

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 66 citations in OpenAlex.

  1. Considerations for early life genetic therapies in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  2. Paranasal Sinus CT and Polysomnographic Findings in Adults with Cystic Fibrosis: Implications for Obstructive Sleep Apnea.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Fibrocyte accumulation in the lungs of cystic fibrosis patients.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014
    Review
  17. Article
  18. Article
  19. Article
  20. Association of CFTR gene mutation with bronchial asthma.The Indian journal of medical research · 2012
    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

7 authors at 3 institutions in 1 country.

Clarisse VandebrouckInstitut de Physiologie et Biologie Cellulaires CNRS UMR 6187, Université de Poitiers, 40 Avenue du Recteur Pineau 86022 Poitiers, Cedex, France. clarisse.vandebrouck@univ-poitiers.fr
Patricia Melin
Caroline Norez
Renaud Robert
Christelle Guibert
Yvette Mettey
Frédéric Becq
Centre National de la Recherche Scientifique · FRUniversité de Poitiers · FRLaboratoire de Physiologie Cellulaire

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe airway functions are profoundly affected in many diseases including asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF). CF the most common lethal autosomal recessive genetic disease is caused by mutations of the CFTR gene, which normally encodes a multifunctional and integral membrane protein, the CF transmembrane conductance regulator (CFTR) expressed in airway epithelial cells.

methodsTo demonstrate that CFTR is also expressed in tracheal smooth muscle cells (TSMC), we used iodide efflux assay to analyse the chloride transports in organ culture of rat TSMC, immunofluorescence study to localize CFTR proteins and isometric contraction measurement on isolated tracheal rings to observe the implication of CFTR in the bronchodilation.

resultsWe characterized three different pathways stimulated by the cAMP agonist forskolin and the isoflavone agent genistein, by the calcium ionophore A23187 and by hypo-osmotic challenge. The pharmacology of the cAMP-dependent iodide efflux was investigated in detail. We demonstrated in rat TSMC that it is remarkably similar to that of the epithelial CFTR, both for activation (using three benzo [c]quinolizinium derivatives) and for inhibition (glibenclamide, DPC and CFTRinh-172). Using rat tracheal rings, we observed that the activation of CFTR by benzoquinolizinium derivatives in TSMC leads to CFTRinh-172-sensitive bronchodilation after constriction with carbachol. An immunolocalisation study confirmed expression of CFTR in tracheal myocytes.

conclusionAltogether, these observations revealed that CFTR in the airways of rat is expressed not only in the epithelial cells but also in tracheal smooth muscle cells leading to the hypothesis that this ionic channel could contribute to bronchodilation.

Indexed as

AnimalsBronchoconstrictionCells, CulturedChlorineCystic Fibrosis Transmembrane Conductance RegulatorGene ExpressionIn Vitro TechniquesIsometric ContractionMyocytes, Smooth MuscleRatsRats, WistarSignal TransductionTracheaChlorineCystic Fibrosis Transmembrane Conductance Regulator

Identifiers

PMID16938132
PMCPMC1560124
OpenAlexW2163267347

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.