Evidence map›Paper›PMID 16968555›Full record

ArticleCritical care (London, England)2006

The early responses of VEGF and its receptors during acute lung injury: implication of VEGF in alveolar epithelial cell survival.

Marco Mura, Bing Han, Cristiano F Andrade, Rashmi Seth, David Hwang, Thomas K Waddell, Shaf Keshavjee, Mingyao Liu

Open access · goldAbstract readComparative Study
In one paragraph

Article in Critical care (London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
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  15. Peripheral Circulating Exosome-Mediated Delivery of miR-155 as a Novel Mechanism for Acute Lung Inflammation.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  16. Article
  17. VEGF (Vascular Endothelial Growth Factor) and Fibrotic Lung Disease.International journal of molecular sciences · 2018
    Review
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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

8 authors at 2 institutions in 1 country.

Marco MuraThoracic Surgery Research Laboratories, Toronto General Research Institute, University Health Network, Toronto, Canada M5G 2C4.
Bing Han
Cristiano F Andrade
Rashmi Seth
David Hwang
Thomas K Waddell
Shaf Keshavjee
Mingyao Liu
University of Toronto · CAUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe function of the vascular endothelial growth factor (VEGF) system in acute lung injury (ALI) is controversial. We hypothesized that the role of VEGF in ALI may depend upon the stages of pathogenesis of ALI.

methodsTo determine the responses of VEGF and its receptors during the early onset of ALI, C57BL6 mice were subjected to intestinal ischemia or sham operation for 30 minutes followed by intestinal ischemia-reperfusion (IIR) for four hours under low tidal volume ventilation with 100% oxygen. The severity of lung injury, expression of VEGF and its receptors were assessed. To further determine the role of VEGF and its type I receptor in lung epithelial cell survival, human lung epithelial A549 cells were treated with small interference RNA (siRNA) to selectively silence related genes.

resultsIIR-induced ALI featured interstitial inflammation, enhancement of pulmonary vascular permeability, increase of total cells and neutrophils in the bronchoalveolar lavage (BAL), and alveolar epithelial cell death. In the BAL, VEGF was significantly increased in both sham and IIR groups, while the VEGF and VEGF receptor (VEGFR)-1 in the lung tissues were significantly reduced in these two groups. The increase of VEGF in the BAL was correlated with the total protein concentration and cell count. Significant negative correlations were observed between the number of VEGF or VEGFR-1 positive cells, and epithelial cells undergoing cell death. When human lung epithelial A549 cells were pre-treated with 50 nM of siRNA either against VEGF or VEGFR-1 for 24 hours, reduced VEGF and VEGFR-1 levels were associated with reduced cell viability.

conclusionThese results suggest that VEGF may have dual roles in ALI: early release of VEGF may increase pulmonary vascular permeability; reduced expression of VEGF and VEGFR-1 in lung tissue may contribute to the death of alveolar epithelial cells.

Indexed as

AnimalsCell DeathCell SurvivalMaleMiceMice, Inbred C57BLPulmonary AlveoliReceptors, Vascular Endothelial Growth FactorRespiratory Distress SyndromeRespiratory MucosaTime FactorsVascular Endothelial Growth Factor AReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor A

Identifiers

PMID16968555
PMCPMC1751039
OpenAlexW1534580282

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.