Evidence map›Paper›PMID 24941004›Full record

ArticlePloS one2014

Effect of P2X7 receptor knockout on AQP-5 expression of type I alveolar epithelial cells.

Georg Ebeling, Robert Bläsche, Falk Hofmann, Antje Augstein, Michael Kasper, Kathrin Barth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. In focus in HCB.Histochemistry and cell biology · 2018
    Article
  8. Review
  9. Article
  10. Purinergic signaling in scarring.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Review
  11. Article
  12. 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

6 authors at 1 institution in 1 country.

Georg EbelingInstitute of Anatomy, Medical Faculty Carl Custav Carus, Technische Universität Dresden, Dresden, Germany.
Robert BläscheInstitute of Anatomy, Medical Faculty Carl Custav Carus, Technische Universität Dresden, Dresden, Germany.
Falk HofmannInstitute of Anatomy, Medical Faculty Carl Custav Carus, Technische Universität Dresden, Dresden, Germany.
Antje AugsteinDepartment of Internal Medicine and Cardiology, Technische Universität Dresden, Dresden, Germany.
Michael KasperInstitute of Anatomy, Medical Faculty Carl Custav Carus, Technische Universität Dresden, Dresden, Germany.
Kathrin BarthInstitute of Anatomy, Medical Faculty Carl Custav Carus, Technische Universität Dresden, Dresden, Germany.
TU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P2X7 receptors, ATP-gated cation channels, are specifically expressed in alveolar epithelial cells. The pathophysiological function of this lung cell type, except a recently reported putative involvement in surfactant secretion, is unknown. In addition, P2X7 receptor-deficient mice show reduced inflammation and lung fibrosis after exposure with bleomycin. To elucidate the role of the P2X7 receptor in alveolar epithelial type I cells we characterized the pulmonary phenotype of P2X7 receptor knockout mice by using immunohistochemistry, western blot analysis and real-time RT PCR. No pathomorphological signs of fibrosis were found. Results revealed, however, a remarkable loss of aquaporin-5 protein and mRNA in young knockout animals. Additional in vitro experiments with bleomycin treated precision cut lung slices showed a greater sensitivity of the P2X7 receptor knockout mice in terms of aquaporin-5 reduction as wild type animals. Finally, P2X7 receptor function was examined by using the alveolar epithelial cell lines E10 and MLE-12 for stimulation experiments with bleomycin. The in vitro activation of P2X7 receptor was connected with an increase of aquaporin-5, whereas the inhibition of the receptor with oxidized ATP resulted in down regulation of aquaporin-5. The early loss of aquaporin-5 which can be found in different pulmonary fibrosis models does not implicate a specific pathogenetic role during fibrogenesis.

Indexed as

Adenosine TriphosphateAnimalsAquaporin 5BleomycinCell LineEpithelial CellsGene Expression RegulationMiceMice, KnockoutPulmonary AlveoliPulmonary FibrosisReceptors, Purinergic P2X7RNA, MessengerSignal TransductionTissue Culture Techniques2',3'-dialdehyde ATPAdenosine TriphosphateAqp5 protein, mouseAquaporin 5BleomycinReceptors, Purinergic P2X7RNA, Messenger

Identifiers

PMID24941004
PMCPMC4062497
OpenAlexW2056705474

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.