Evidence map›Paper›PMID 16400009›Full record

ArticleThe American journal of pathology2006

alpha3alpha5beta2-Nicotinic acetylcholine receptor contributes to the wound repair of the respiratory epithelium by modulating intracellular calcium in migrating cells.

Jean-Marie Tournier, Kamel Maouche, Christelle Coraux, Jean-Marie Zahm, Isabelle Cloëz-Tayarani, Béatrice Nawrocki-Raby, Arnaud Bonnomet, Henriette Burlet, François Lebargy, Myriam Polette and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Ly6/uPAR Protein fromMarine drugs · 2025
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  10. Contribution of α7 nicotinic receptor to airway epithelium dysfunction under nicotine exposure.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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 2 institutions in 1 country.

Jean-Marie TournierINSERM UMRS-514, 45 rue Cognacq-Jay, 51092 Reims Cedex, France. jm.tournier@univ-reims.fr
Kamel Maouche
Christelle Coraux
Jean-Marie Zahm
Isabelle Cloëz-Tayarani
Béatrice Nawrocki-Raby
Arnaud Bonnomet
Henriette Burlet
François Lebargy
Myriam Polette
Philippe Birembaut
Inserm · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicotinic acetylcholine receptors (nAChRs), present in human bronchial epithelial cells (HBECs), have been shown in vitro to modulate cell shape. Because cell spreading and migration are important mechanisms involved in the repair of the bronchial epithelium, we investigated the potential role of nAChRs in the wound repair of the bronchial epithelium. In vivo and in vitro, alpha3alpha5beta2-nAChRs accumulated in migrating HBECs involved in repairing a wound, whereas alpha7-nAChRs were predominantly observed in stationary confluent cells. Wound repair was improved in the presence of nAChR agonists, nicotine, and acetylcholine, and delayed in the presence of alpha3beta2 neuronal nAChR antagonists, mecamylamine, alpha-conotoxin MII, and kappa-bungarotoxin; alpha-bungarotoxin, an antagonist of alpha7-nAChR, had no effect. Addition of nicotine to a repairing wound resulted in a dose-dependent transient increase of intracellular calcium in migrating cells that line the wound edge. Mecamylamine and kappa-bungarotoxin inhibited both the cell-migration speed and the nicotine-induced intracellular calcium increase in wound-repairing migrating cells in vitro. On the contrary alpha-bungarotoxin had no significant effect on migrating cells. These results suggest that alpha3alpha5beta2-nAChRs actively contribute to the wound repair process of the respiratory epithelium by modulating intracellular calcium in wound-repairing migrating cells.

Indexed as

AgedAged, 80 and overCalciumCell MovementCells, CulturedHumansImmunoblottingImmunohistochemistryIntracellular FluidMiddle AgedNicotineNicotinic AntagonistsReceptors, NicotinicRespiratory MucosaReverse Transcriptase Polymerase Chain ReactionWound HealingCalciumNicotineNicotinic AntagonistsReceptors, Nicotinic

Identifiers

PMID16400009
PMCPMC1592670
OpenAlexW2160167217

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.