Evidence map›Paper›PMID 17322107›Full record

ArticleAmerican journal of respiratory and critical care medicine2007

Blocking p21-activated kinase reduces lipopolysaccharide-induced acute lung injury by preventing polymorphonuclear leukocyte infiltration.

Jörg Reutershan, Rebecca Stockton, Alexander Zarbock, Gail W Sullivan, Daniel Chang, David Scott, Martin A Schwartz, Klaus Ley

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2007. 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
1.8field-weighted citation impact, top 15% 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, 43 citations in OpenAlex.

  1. Article
  2. Sinner or Saint?: Nck Adaptor Proteins in Vascular Biology.Frontiers in cell and developmental biology · 2021
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  3. Review
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  6. Neutrophil-endothelial interactions of murine cells is not a good predictor of their interactions in human cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  7. RNAi therapeutic strategies for acute respiratory distress syndrome.Translational research : the journal of laboratory and clinical medicine · 2019
    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 4 institutions in 4 countries.

Jörg ReutershanRobert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908-1394, USA.
Rebecca Stockton
Alexander Zarbock
Gail W Sullivan
Daniel Chang
David Scott
Martin A Schwartz
Klaus Ley
University of Virginia · USInstitute of Biophysics and Biomedical Engineering · BGTH Bingen University of Applied Sciences · DEUniversity of Münster · DE

Funding

ROLE OF INFLAMMATION IN PULMONARY INJURYP01HL073361 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MEHRAD, BORNA · 2004 to 2008
$8.0M
Integrins in the Endothelial Response to Fluid Shear StressR01HL075092 · NHLBI · YALE UNIVERSITY · PI SCHWARTZ, MARTIN A · 2004 to 2019
$5.1M
Inflammation in Vein Graft Disease: A Genetic ApproachR01HL072842 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI PEPPEL, KARSTEN · 2004 to 2007
$1.5M
NHLBI NIH HHS 5T32 HL-72842-27NHLBI NIH HHS HL73361NHLBI NIH HHS HL75092
6 · The paper itself

Abstract

rationaleExcessive recruitment of polymorphonuclear leukocytes (PMNs) to the lung promotes acute lung injury (ALI). Chemokine receptors and adhesion molecules initiate leukocyte-endothelial interactions, but mediators of PMN migration through the alveolo-capillary membrane remain to be identified. p21-Activated kinase (PAK) is an effector of small GTPases and has been implicated in cell migration.

objectivesTo test the role of PAK in ALI.

methodsAn inhibitory PAK peptide was used to determine the role of PAK in cytoskeletal actin polymerization, cell adhesion, and oxidative burst. PMN migration was investigated in vitro and in a murine model of lipopolysaccharide-induced lung injury. MEASUREMENTS AND MAIN

resultsPMN migration into lung interstitium and alveolar space was suppressed by an inhibitory PAK peptide. Neutrophils that had taken up the inhibitory PAK peptide were unable to enter the alveolar space. CXCL2/3, an important PMN chemoattractant in murine lung injury, induced PAK phosphorylation in PMNs. Blocking PAK function inhibited chemotaxis, chemokine-induced cytoskeletal actin polymerization, and adhesion-induced oxidative burst.

conclusionsWe conclude that neutrophil PAK is a critical mediator of PMN migration and may be an attractive target in ALI.

Indexed as

Chemotaxis, LeukocyteActinsAnimalsCell AdhesionChemokines, CXCHumansLipopolysaccharidesMacrophagesMiceNeutrophilsp21-Activated KinasesPeptidesPhosphorylationProtein Serine-Threonine KinasesReceptors, Interleukin-8BRespiratory BurstActinsChemokines, CXCCXCL3 protein, humanLipopolysaccharidesp21-Activated KinasesPAK1 protein, humanPak1 protein, mousePeptidesProtein Serine-Threonine KinasesReceptors, Interleukin-8B

Identifiers

PMID17322107
PMCPMC1899271
OpenAlexW2161413176

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.