Evidence map›Paper›PMID 19461051›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2009

Inhibition of VEGF or TGF-{beta} signaling activates endothelium and increases leukocyte rolling.

Tony E Walshe, Vandana S Dole, Arindel S R Maharaj, Ian S Patten, Denisa D Wagner, Patricia A D'Amore

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.6field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

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  16. Bone Morphogenetic Proteins in Vascular Homeostasis and Disease.Cold Spring Harbor perspectives in biology · 2018
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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 1 institution in 1 country.

Tony E WalsheSchepens Eye Research Institute and Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.
Vandana S Dole
Arindel S R Maharaj
Ian S Patten
Denisa D Wagner
Patricia A D'Amore
Massachusetts Eye and Ear Infirmary · US

Funding

Platelets in Cardiovascular Biology and PathologyP01HL066105 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HYNES, RICHARD O · 2001 to 2010
$28.4M
THE ROLE OF MICROVASCULAR CELLS IN NEOVASCULARIZATIONR01EY005318 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI D'AMORE, PATRICIA ANN · 1985 to 2015
$6.4M
NEI NIH HHS EY05318NEI NIH HHS R01 EY005318NHLBI NIH HHS P01 HL066105NHLBI NIH HHS P0I HL066105
6 · The paper itself

Abstract

objectiveMotivated by the central roles that vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)-beta play in the assembly and maintenance of the vasculature, we examined the impact of systemic VEGF or TGF-beta signal inhibition on endothelial activation as detected by leukocyte-endothelial interactions. METHODS AND

resultsVEGF or TGF-beta inhibition, accomplished using adenovirus expression of soluble Flt1 (Ad-sFlt1) or soluble endoglin (Ad-sEng), resulted in a significant increase in the number of leukocytes rolling along the mesenteric venous endothelium and a significant decrease in rolling velocity in Ad-sEng mice. Neutralization of VEGF or TGF-beta resulted in endothelial surface expression of P-selectin and impaired peripheral vasodilatation. Neither inhibition of VEGF nor TGF-beta was associated with platelet or leukocyte activation, as detected by the activation markers platelet P-selectin and the active integrin alphaIIbbetaIII, or by leukocyte expression of L-selectin. Soluble vascular cell adhesion molecule (VCAM)-1 and E-selectin were increased in sEng-expressing mice, indicating higher levels of these adhesion receptors.

conclusionsVEGF or TGF-beta neutralization leads to impaired endothelium-mediated vasodilatation and elevated expression of surface adhesion molecules, resulting in increased leukocyte adhesion. These results indicate an essential role for both VEGF and TGF-beta in maintaining the endothelium in a nonactivated state and have implications for therapeutic approaches that neutralize VEGF or TGF-beta.

Indexed as

AnimalsCell AdhesionEndothelium, VascularE-SelectinLeukocyte CountLeukocytesMesenteric VeinsMiceMice, Inbred BALB CP-SelectinSignal TransductionTransforming Growth Factor betaVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor AVasodilationE-SelectinP-SelectinTransforming Growth Factor betaVascular Cell Adhesion Molecule-1Vascular Endothelial Growth Factor A

Identifiers

PMID19461051
PMCPMC2775449
OpenAlexW2031117727

What OpenQuestion holds

Textmetadata
LicenceTDM
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.