Evidence map›Paper›PMID 11337375›Full record

ArticleThe American journal of pathology2001

Regulation of gap junctional communication by a pro-inflammatory cytokine in cystic fibrosis transmembrane conductance regulator-expressing but not cystic fibrosis airway cells.

M Chanson, P Y Berclaz, I Scerri, T Dudez, K Wernke-Dollries, L Pizurki, A Pavirani, M A Fiedler, S Suter

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Role of ROS/RNS in Preeclampsia: Are Connexins the Missing Piece?International journal of molecular sciences · 2020
    Review
  5. Article
  6. Article
  7. Review
  8. The lung communication network.Cellular and molecular life sciences : CMLS · 2015
    Review
  9. Article
  10. Review
  11. Article
  12. Sensitivity of chloride efflux vs. transepithelial measurements in mixed CF and normal airway epithelial cell populations.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2010
    Article
  13. DNA-triggered innate immune responses are propagated by gap junction communication.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  14. Article
  15. Article
  16. TLR2 regulates gap junction intercellular communication in airway cells.Journal of immunology (Baltimore, Md. : 1950) · 2008
    Article
  17. Is there a role for remodeled connexins in AF? No simple answers.Journal of molecular and cellular cardiology · 2008
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

M ChansonDepartment of Pediatrics, Laboratory of Clinical Investigation III, University Hopitals, Geneva, Switzerland. marc_chanson@hotmail.com
P Y Berclaz
I Scerri
T Dudez
K Wernke-Dollries
L Pizurki
A Pavirani
M A Fiedler
S Suter
University Hospital of Geneva · CHBoston Children's Hospital · USTransgene (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway inflammation is orchestrated by cell-cell interactions involving soluble mediators and cell adhesion molecules. Alterations in the coordination of the multicellular process of inflammation may play a major role in the chronic lung disease state of cystic fibrosis (CF). The aim of this study was to determine whether direct cell-cell interactions via gap junctional communication is affected during the inflammatory response of the airway epithelium. We have examined the strength of intercellular communication and the activation of nuclear factor-kappaB (NF-kappaB) in normal (non-CF) and CF human airway cell lines stimulated with tumor necrosis factor-alpha (TNF-alpha). TNF-alpha induced maximal translocation of NF-kappaB into the nucleus of non-CF as well as CF airway cells within 20 minutes. In non-CF cells, TNF-alpha progressively decreased the extent of intercellular communication. In contrast, gap junctional communication between CF cells exposed to TNF-alpha remained unaltered. CF results from mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Interestingly, transfer of wild-type CFTR into CF cells by adenovirus-mediated infection was associated with the recovery of TNF-alpha-induced uncoupling. These results suggest that expression of functional CFTR is necessary for regulation of gap junctional communication by TNF-alpha. Gap junction channels close during the inflammatory response, therefore limiting the intercellular diffusion of signaling molecules, and thereby the recruitment of neighboring cells. Defects in this mechanism may contribute to the excessive inflammatory response of CF airway epithelium.

Indexed as

BronchiCell CommunicationCell LineConnexinsCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorCytokinesFluorescent DyesGap JunctionsGene Expression RegulationHumansIsoquinolinesNF-kappa BRNA, MessengerTumor Necrosis Factor-alphaCFTR protein, humanConnexinsCystic Fibrosis Transmembrane Conductance RegulatorCytokinesFluorescent DyesIsoquinolineslucifer yellowNF-kappa BRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID11337375
PMCPMC1891964
OpenAlexW2029937137

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.