Evidence map›Paper›PMID 22303475›Full record

ArticlePloS one2012

A role for VEGFR2 activation in endothelial responses caused by barrier disruptive OxPAPC concentrations.

Anna A Birukova, Sangderk Lee, Vitaliy Starosta, Tinghuai Wu, Tiffany Ho, Jin Kim, Judith A Berliner, Konstantin G Birukov

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  6. Antioxidants (Basel, Switzerland) · 2021
    Article
  7. Review
  8. Induced dysregulation of ACE2 by SARS-CoV-2 plays a key role in COVID-19 severity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
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  14. Elevated truncated oxidized phospholipids as a factor exacerbating ALI in the aging lungs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  15. Review
  16. Article
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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.

Anna A BirukovaSection of Pulmonary and Critical Medicine, Department of Medicine, Lung Injury Center, University of Chicago, Chicago, Illinois, United States of America.
Sangderk Lee
Vitaliy Starosta
Tinghuai Wu
Tiffany Ho
Jin Kim
Judith A Berliner
Konstantin G Birukov
University of California, Los Angeles · USUniversity of Chicago · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
Tissue Culture Biomechanical CoreP01HL058064 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAL, RATNESHWAR · 1998 to 2012
$27.8M
Control of Lung Permeability by Oxidized PhospholipidsR01HL076259 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2004 to 2023
$6.8M
Molecular control of lung endothelial barrier function in ALIR01HL087823 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOV, KONSTANTIN · 2008 to 2020
$4.6M
Microtubule-associated regulation of acute lung injuryR01HL107920 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BIRUKOVA, ANNA · 2011 to 2019
$2.8M
Protective role of ANP in the models of acute lung injuryR01HL089257 · NHLBI · UNIVERSITY OF CHICAGO · PI BIRUKOVA, ANNA · 2009 to 2013
$1.9M
Role of MP-HBEGF-EGFR signaling for inflammatory action of oxidized phospholipidsR00HL105577 · NHLBI · UNIVERSITY OF KENTUCKY · PI LEE, SANGDERK · 2013 to 2015
$718k
Microtubule-associated regulation of acute lung injuryR56HL107920 · NHLBI · UNIVERSITY OF CHICAGO · PI BIRUKOVA, ANNA · 2015 to 2015
$395k
Role of MP-HBEGF-EGFR signaling for inflammatory action of oxidized phospholipidsK99HL105577 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEE, SANGDERK · 2011 to 2012
$180k
NHLBI NIH HHS HL107920NHLBI NIH HHS HL76259NHLBI NIH HHS HL87823NHLBI NIH HHS HL89257NHLBI NIH HHS K99 HL105577NHLBI NIH HHS K99HL105577NHLBI NIH HHS P01 HL030568NHLBI NIH HHS P01 HL058064NHLBI NIH HHS P01 HL58064NHLBI NIH HHS R00 HL105577NHLBI NIH HHS R01 HL076259NHLBI NIH HHS R01 HL087823NHLBI NIH HHS R01 HL089257NHLBI NIH HHS R01 HL107920NHLBI NIH HHS R56 HL107920
6 · The paper itself

Abstract

introductionOxidation products of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphatidylcholine (OxPAPC) differentially modulate endothelial cell (EC) barrier function in a dose-dependent fashion. Vascular endothelial growth factor receptor-2 (VEGFR2) is involved in the OxPAPC-induced EC inflammatory activation. This study examined a role of VEGFR2 in barrier dysfunction caused by high concentrations of OxPAPC and evaluated downstream signaling mechanisms resulting from the effect of OxPAPC in EC from pulmonary and systemic circulation.

methodsEC monolayer permeability in human pulmonary artery endothelial cells (HPAEC) and human aortic endothelial cells (HAEC) was monitored by changes in transendothelial electrical resistance (TER) across EC monolayers. Actin cytoskeleton was examined by immunostaining with Texas Red labeled phalloidin. Phosphorylation of myosin light chains (MLC) and VE-Cadherin was examined by Western blot and immunofluorescence techniques. The role of VEGFR2 in OxPAPC-induced permeability and cytoskeletal arrangement were determined using siRNA-induced VEGFR2 knockdown.

resultsLow OxPAPC concentrations (5-20 µg/ml) induced a barrier protective response in both HPAEC and HAEC, while high OxPAPC concentrations (50-100 µg/ml) caused a rapid increase in permeability; actin stress fiber formation and increased MLC phosphorylation were observed as early as 30 min after treatment. VEGFR2 knockdown dramatically decreased the amount of MLC phosphorylation and stress fiber formation caused by high OxPAPC concentrations with modest effects on the amount of VE-cadherin phosphorylation at Y(731). We present evidence that activation of Rho is involved in the OxPAPC/VEGFR2 mechanism of EC permeability induced by high OxPAPC concentrations. Knockdown of VEGFR2 did not rescue the early drop in TER but prevented further development of OxPAPC-induced barrier dysfunction.

conclusionsThis study shows that VEGFR2 is involved in the delayed phase of EC barrier dysfunction caused by high OxPAPC concentrations and contributes to stress fiber formation and increased MLC phosphorylation.

Indexed as

Actin CytoskeletonAntigens, CDAortaCadherin 5CadherinsCell Membrane PermeabilityElectric ImpedanceEndothelial CellsEnzyme ActivationHumansIntracellular SpaceMyosin Light ChainsPhosphatidylcholinesProtein TransportPulmonary Arteryrac GTP-Binding ProteinsAntigens, CDCadherin 5CadherinsMyosin Light Chainsoxidized-L-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholinePhosphatidylcholinesrac GTP-Binding Proteinsrho GTP-Binding ProteinsVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID22303475
PMCPMC3269437
OpenAlexW1968948763

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.