Evidence map›Paper›PMID 21812913›Full record

ArticleJournal of thrombosis and haemostasis : JTH2011

Splice variants of tissue factor promote monocyte-endothelial interactions by triggering the expression of cell adhesion molecules via integrin-mediated signaling.

R Srinivasan, E Ozhegov, Y W van den Berg, B J Aronow, R S Franco, M B Palascak, J T Fallon, W Ruf, H H Versteeg, V Y Bogdanov

Open access · bronzeAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 69 citations in OpenAlex.

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  18. Activation of carbonic anhydrase IX by alternatively spliced tissue factor under late-stage tumor conditions.Laboratory investigation; a journal of technical methods and pathology · 2016
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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

10 authors at 5 institutions in 2 countries.

R SrinivasanDivision of Hematology/Oncology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
E Ozhegov
Y W van den Berg
B J Aronow
R S Franco
M B Palascak
J T Fallon
W Ruf
H H Versteeg
V Y Bogdanov
University of Cincinnati Medical Center · USLeiden University Medical Center · NLCincinnati Children's Hospital Medical Center · USNew York Medical College · USScripps Research Institute · US

Funding

Inducible transgenes expressing EJC enriched mRNAs: a post-genomic innovationR21HL094891 · NHLBI · UNIVERSITY OF CINCINNATI · PI BOGDANOV, VLADIMIR · 2009 to 2010
$428k
NHLBI NIH HHS HL094891NHLBI NIH HHS R21 HL094891
6 · The paper itself

Abstract

backgroundTF is highly expressed in cancerous and atherosclerotic lesions. Monocyte recruitment is a hallmark of disease progression in these pathological states.

objectiveTo examine the role of integrin signaling in TF-dependent recruitment of monocytes by endothelial cells.

methodsThe expression of flTF and asTF in cervical cancer and atherosclerotic lesions was examined. Biologic effects of the exposure of primary microvascular endothelial cells (MVEC) to truncated flTF ectodomain (LZ-TF) and recombinant asTF were assessed.

resultsflTF and asTF exhibited nearly identical expression patterns in cancer lesions and lipid-rich plaques. Tumor lesions, as well as stromal CD68(+)  monocytes/macrophages, expressed both TF forms. Primary MVEC rapidly adhered to asTF and LZ-TF, and this was completely blocked by anti-β1 integrin antibody. asTF- and LZ-TF-treatment of MVEC promoted adhesion of peripheral blood mononuclear cells (PBMCs) under orbital shear conditions and under laminar flow; asTF-elicited adhesion was more pronounced than that elicited by LZ-TF. Expression profiling and western blotting revealed a broad activation of cell adhesion molecules (CAMs) in MVEC following asTF treatment including E-selectin, ICAM-1 and VCAM-1. In transwell assays, asTF potentiated PMBC migration through MVEC monolayers by ∼3-fold under MCP-1 gradient.

conclusionsTF splice variants ligate β1 integrins on MVEC, which induces the expression of CAMs in MVEC and leads to monocyte adhesion and transendothelial migration. asTF appears more potent than flTF in eliciting these effects. Our findings underscore the pathophysiologic significance of non-proteolytic, integrin-mediated signaling by the two naturally occurring TF variants in cancer and atherosclerosis.

Indexed as

Alternative SplicingSignal TransductionBlotting, WesternCell Adhesion MoleculesCells, CulturedEndothelium, VascularFemaleHumansIntegrinsMonocytesReverse Transcriptase Polymerase Chain ReactionThromboplastinUterine Cervical NeoplasmsCell Adhesion MoleculesIntegrinsThromboplastin

Identifiers

PMID21812913
PMCPMC3292430
OpenAlexW1576346631

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.