Evidence map›Paper›PMID 23980650›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Neutrophil-endothelial interactions mediate angiopoietin-2-associated pulmonary endothelial cell dysfunction in indirect acute lung injury in mice.

Joanne Lomas-Neira, Fabienne Venet, Chun-Shiang Chung, Rajan Thakkar, Daithi Heffernan, Alfred Ayala

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  7. Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024
    Review
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  14. Observational
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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

6 authors at 2 institutions in 2 countries.

Joanne Lomas-Neira1 Division of Surgical Research, Department of Surgery, Rhode Island Hospital/Alpert School of Medicine at Brown University, Providence, Rhode Island; and.
Fabienne Venet
Chun-Shiang Chung
Rajan Thakkar
Daithi Heffernan
Alfred Ayala
Brown University · USHospices Civils de Lyon · FR

Funding

Uncoupling of IL-1 beta and VEGF-A Crosstalk Contributes to Impaired Arteriogenesis Response to Ischemia in Chronic Diabetes MellitusP20GM103652 · NIGMS · OCEAN STATE RESEARCH INSTITUTE, INC. · PI ZHOU, YANG · 2013 to 2022
$21.3M
Co-Inhibitory Molecules and the Pathology of Indirect-Acute Lung InjuryR01GM107149 · NIGMS · RHODE ISLAND HOSPITAL · PI AYALA, ALFRED · 2013 to 2015
$906k
NIGMS NIH HHS P20 GM103652NIGMS NIH HHS P20-GM103652-01A1NIGMS NIH HHS R01 GM107149NIGMS NIH HHS R01-GM107149-01
6 · The paper itself

Abstract

Unresolved inflammation in the lung is thought to elicit loss of endothelial cell (EC) barrier integrity and impaired lung function. We have shown, in a mouse model of shock/sepsis, that neutrophil interactions with resident pulmonary cells appear central to the pathogenesis of indirect acute lung injury (iALI). Normally, EC growth factors angiopoietin (Ang)-1 and Ang-2 maintain vascular homeostasis through tightly regulated interaction with the kinase receptor Tie2 expressed on ECs. Although Ang-1/Tie2 has been shown to promote vessel integrity, stimulating downstream prosurvival/antiinflammatory signaling, Ang-2, released from activated ECs, is reported to promote vessel destabilization. This mechanism of regulation, together with recent clinical findings that plasma Ang-2 levels are significantly elevated in patients who develop acute respiratory distress syndrome, has focused our investigation on the contribution of Ang-2 to the development of iALI. A murine model of hemorrhagic shock-induced priming for the development of iALI after subsequent septic challenge was used in this study. Our findings show that 1) Ang-2 is elevated in our experimental model for iALI, 2) direct EC/neutrophil interactions contribute significantly to EC Ang-2 release, and 3) suppression of Ang-2 significantly decreases inflammatory lung injury, neutrophil influx, and lung and plasma IL-6 and TNF-α. These findings support our hypothesis and suggest that Ang-2 plays a role in the loss of pulmonary EC barrier function in the development of iALI in mice resultant from the sequential insults of hemorrhagic shock and sepsis and that this is mediated by EC interaction with activated neutrophils.

Indexed as

Acute Lung InjuryAngiopoietin-2AnimalsCells, CulturedEndothelial CellsHumansInflammationInterleukin-6LungMaleMiceMice, Inbred C57BLNeutrophilsSepsisShock, HemorrhagicTumor Necrosis Factor-alphaAngiopoietin-2Interleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID23980650
PMCPMC3930935
OpenAlexW2158725913

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.