Evidence map›Paper›PMID 22087324›Full record

ArticlePloS one2011

The role of purinergic signaling on deformation induced injury and repair responses of alveolar epithelial cells.

Hewan A Belete, Rolf D Hubmayr, Shaohua Wang, Raman-Deep Singh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of the Purinergic P2Y2 Receptor in Pulmonary Hypertension.International journal of environmental research and public health · 2021
    Review
  4. Review
  5. Review
  6. P2 Purinergic Signaling in the Distal Lung in Health and Disease.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Inhaled TRIM72 Protein Protects Ventilation Injury to the Lung through Injury-guided Cell Repair.American journal of respiratory cell and molecular biology · 2018
    Article
  12. Observational
  13. Review
  14. ATP is stored in lamellar bodies to activate vesicular P2XThe Journal of general physiology · 2018
    Article
  15. Review
  16. Plasma membrane wounding and repair in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  17. Review
  18. Article
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Hewan A BeleteThoracic Diseases Research Unit, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota, United States of America.
Rolf D Hubmayr
Shaohua Wang
Raman-Deep Singh
Mayo Clinic in Florida · US

Funding

MECHANICS AND DEFORMATION RESPONSES OF LUNG CELLSR01HL063178 · NHLBI · MAYO CLINIC ROCHESTER · PI HUBMAYR, ROLF D · 2000 to 2011
$4.2M
NHLBI NIH HHS HL 63178NHLBI NIH HHS R01 HL063178
6 · The paper itself

Abstract

Cell wounding is an important driver of the innate immune response of ventilator-injured lungs. We had previously shown that the majority of wounded alveolus resident cells repair and survive deformation induced insults. This is important insofar as wounded and repaired cells may contribute to injurious deformation responses commonly referred to as biotrauma. The central hypothesis of this communication states that extracellular adenosine-5' triphosphate (ATP) promotes the repair of wounded alveolus resident cells by a P2Y2-Receptor dependent mechanism. Using primary type 1 alveolar epithelial rat cell models subjected to micropuncture injury and/or deforming stress we show that 1) stretch causes a dose dependent increase in cell injury and ATP media concentrations; 2) enzymatic depletion of extracellular ATP reduces the probability of stretch induced wound repair; 3) enriching extracellular ATP concentrations facilitates wound repair; 4) purinergic effects on cell repair are mediated by ATP and not by one of its metabolites; and 5) ATP mediated cell salvage depends at least in part on P2Y2-R activation. While rescuing cells from wounding induced death may seem appealing, it is possible that survivors of membrane wounding become governors of a sustained pro-inflammatory state and thereby perpetuate and worsen organ function in the early stages of lung injury syndromes. Means to uncouple P2Y2-R mediated cytoprotection from P2Y2-R mediated inflammation and to test the preclinical efficacy of such an undertaking deserve to be explored.

Indexed as

Adenosine TriphosphateAnimalsEpithelial CellsImmunity, InnateInflammationPulmonary AlveoliRatsReceptors, Purinergic P2Y2Signal TransductionWound HealingAdenosine TriphosphateReceptors, Purinergic P2Y2

Identifiers

PMID22087324
PMCPMC3210789
OpenAlexW1983414601

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.