Evidence map›Paper›PMID 21724858›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

Balance of life and death in alveolar epithelial type II cells: proliferation, apoptosis, and the effects of cyclic stretch on wound healing.

Lynn M Crosby, Charlean Luellen, Zhihong Zhang, Larry L Tague, Scott E Sinclair, Christopher M Waters

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In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. An Agent-Based Model of Radiation-Induced Lung Fibrosis.International journal of molecular sciences · 2022
    Article
  5. Article
  6. Human-Based AdvancedFrontiers in medicine · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. TRIM72 is required for effective repair of alveolar epithelial cell wounding.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Measurement of local permeability at subcellular level in cell models of agonist- and ventilator-induced lung injury.Laboratory investigation; a journal of technical methods and pathology · 2013
    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

6 authors at 1 institution in 1 country.

Lynn M CrosbyDepartment of Physiology, University of Tennessee Health Science Center, Memphis, USA.
Charlean Luellen
Zhihong Zhang
Larry L Tague
Scott E Sinclair
Christopher M Waters
University of Tennessee Health Science Center · US

Funding

Mechanotransduction in Acute Lung InjuryR01HL094366 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WATERS, CHRISTOPHER M · 2009 to 2012
$2.1M
NHLBI NIH HHS HL-094366NHLBI NIH HHS R01 HL094366
6 · The paper itself

Abstract

After acute lung injury, repair of the alveolar epithelium occurs on a substrate undergoing cyclic mechanical deformation. While previous studies showed that mechanical stretch increased alveolar epithelial cell necrosis and apoptosis, the impact of cell death during repair was not determined. We examined epithelial repair during cyclic stretch (CS) in a scratch-wound model of primary rat alveolar type II (ATII) cells and found that CS altered the balance between proliferation and cell death. We measured cell migration, size, and density; intercellular gap formation; cell number, proliferation, and apoptosis; cytoskeletal organization; and focal adhesions in response to scratch wounding followed by CS for up to 24 h. Under static conditions, wounds were closed by 24 h, but repair was inhibited by CS. Wounding stimulated cell motility and proliferation, actin and vinculin redistribution, and focal adhesion formation at the wound edge, while CS impeded cell spreading, initiated apoptosis, stimulated cytoskeletal reorganization, and attenuated focal adhesion formation. CS also caused significant intercellular gap formation compared with static cells. Our results suggest that CS alters several mechanisms of epithelial repair and that an imbalance occurs between cell death and proliferation that must be overcome to restore the epithelial barrier.

Indexed as

Stress, PhysiologicalActinsAcute Lung InjuryAlveolar Epithelial CellsAnimalsApoptosisCell CountCell MovementCell ProliferationCell SurvivalCytoskeletonFocal AdhesionsMaleMicroscopyPrimary Cell CultureRatsActinsVinculin

Identifiers

PMID21724858
PMCPMC3191757
OpenAlexW2060721511

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.