Evidence map›Paper›PMID 24748602›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Lung fibroblasts accelerate wound closure in human alveolar epithelial cells through hepatocyte growth factor/c-Met signaling.

Yoko Ito, Kelly Correll, John A Schiel, Jay H Finigan, Rytis Prekeris, Robert J Mason

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.1field-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

38 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Cell Population-resolved Multiomics Atlas of the Developing Lung.American journal of respiratory cell and molecular biology · 2025
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  10. Review
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  12. Article
  13. Life (Basel, Switzerland) · 2021
    Review
  14. Review
  15. Article
  16. Human-Based AdvancedFrontiers in medicine · 2021
    Review
  17. Review
  18. Article
  19. Alveolar heparan sulfate shedding impedes recovery from bleomycin-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2020
    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

6 authors at 3 institutions in 1 country.

Yoko ItoDepartment of Medicine, National Jewish Health, Denver, Colorado; itoy@NJHealth.org.
Kelly CorrellDepartment of Medicine, National Jewish Health, Denver, Colorado;
John A SchielDepartment of Cell and Developmental Biology, University of Colorado, Aurora, Colorado.
Jay H FiniganDepartment of Medicine, National Jewish Health, Denver, Colorado;
Rytis PrekerisDepartment of Cell and Developmental Biology, University of Colorado, Aurora, Colorado.
Robert J MasonDepartment of Medicine, National Jewish Health, Denver, Colorado;
National Jewish Health · USUniversity of Colorado Anschutz Medical Campus · USUniversity of Colorado Denver · US

Funding

ADAM17-NRG-1 Signaling in Acute Lung InjuryR01HL111674 · NHLBI · NATIONAL JEWISH HEALTH · PI FINIGAN, JAMES H · 2012 to 2016
$1.9M
Air/liquid interface cultures for alveolar type II cell differentiationR21HL106112 · NHLBI · NATIONAL JEWISH HEALTH · PI MASON, ROBERT JAMES · 2011 to 2012
$436k
NHLBI NIH HHS HL 106112NHLBI NIH HHS R01 HL111674
6 · The paper itself

Abstract

There are 190,600 cases of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) each year in the United States, and the incidence and mortality of ALI/ARDS increase dramatically with age. Patients with ALI/ARDS have alveolar epithelial injury, which may be worsened by high-pressure mechanical ventilation. Alveolar type II (ATII) cells are the progenitor cells for the alveolar epithelium and are required to reestablish the alveolar epithelium during the recovery process from ALI/ARDS. Lung fibroblasts (FBs) migrate and proliferate early after lung injury and likely are an important source of growth factors for epithelial repair. However, how lung FBs affect epithelial wound healing in the human adult lung has not been investigated in detail. Hepatocyte growth factor (HGF) is known to be released mainly from FBs and to stimulate both migration and proliferation of primary rat ATII cells. HGF is also increased in lung tissue, bronchoalveolar lavage fluid, and serum in patients with ALI/ARDS. Therefore, we hypothesized that HGF secreted by FBs would enhance wound closure in alveolar epithelial cells (AECs). Wound closure was measured using a scratch wound-healing assay in primary human AEC monolayers and in a coculture system with FBs. We found that wound closure was accelerated by FBs mainly through HGF/c-Met signaling. HGF also restored impaired wound healing in AECs from the elderly subjects and after exposure to cyclic stretch. We conclude that HGF is the critical factor released from FBs to close wounds in human AEC monolayers and suggest that HGF is a potential strategy for hastening alveolar repair in patients with ALI/ARDS.

Indexed as

Adenosine TriphosphateCell MovementCells, CulturedEpithelial CellsFibroblastsHepatocyte Growth FactorHumansInterleukin-1alphaInterleukin-1betaProto-Oncogene Proteins c-metPseudopodiaPulmonary AlveoliSignal TransductionWound HealingAdenosine TriphosphateHepatocyte Growth FactorIL1A protein, humanIL1B protein, humanInterleukin-1alphaInterleukin-1betaProto-Oncogene Proteins c-metalveolar epithelial cellshepatocyte growth factorlung fibroblastswound closure

Identifiers

PMID24748602
PMCPMC4080284
OpenAlexW1967141506

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.