Evidence map›Paper›PMID 36696220›Full record

ArticleJournal of thrombosis and haemostasis : JTH2023

The mechanistic and structural role of von Willebrand factor in endotoxemia-enhanced deep vein thrombosis in mice.

Seon Jae Choi, Courtney N Dwyer, Lindsy Rapkin, Matthew Cormier, Charles C T Hindmarch, Kate Nesbitt, Alison Michels, Wilma Hopman, Laura L Swystun, David Lillicrap

Open access · bronzeAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-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

8 citing papers in PubMed, 7 citations in OpenAlex.

  1. Mouse models to study von Willebrand factor in thrombosis: a scoping review.Research and practice in thrombosis and haemostasis · 2026
    Article
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  4. Review
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  8. Von Willebrand factor-inflammation crosstalk in deep vein thrombosis.Journal of thrombosis and haemostasis : JTH · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Seon Jae ChoiDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Courtney N DwyerDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Lindsy RapkinFluidigm Corporation, Markham, Ontario, Canada.
Matthew CormierDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Charles C T HindmarchQueen's Cardiopulmonary Unit, Translational Institute of Medicine, Department of Medicine, Queen's University, Kingston, Ontario, Canada.
Kate NesbittDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Alison MichelsDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Wilma HopmanKingston General Hospital Research Institute, Kingston Health Sciences Centre, Kingston, Ontario, Canada.
Laura L SwystunDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
David LillicrapDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada. Electronic address: david.lillicrap@queensu.ca.
Queen's University · CAFluidigm (Canada) · CAKingston General Hospital · CA

Funding

Zimmerman Program on the Biology of VWDP01HL144457 · NHLBI · VERSITI WISCONSIN, INC. · PI MONTGOMERY, ROBERT R · 2019 to 2023
$13.3M
CIHR FDN154285NHLBI NIH HHS P01 HL144457
6 · The paper itself

Abstract

backgroundAlthough the concept of immunothrombosis has established a link between inflammation and thrombosis, the role of inflammation in the pathogenesis of deep vein thrombosis remains to be fully elucidated. Further, although various constituents of venous thrombi have been identified, their localizations and cellular and molecular interactions are yet to be combined in a single, multiplexed analysis.

objectivesThe objective of this study was to investigate the role of the von Willebrand factor (VWF) in inflammation-associated venous thrombosis. We also performed a proof-of-concept study of imaging mass cytometry to quantitatively and simultaneously analyze the localizations and interactions of 10 venous thrombus constituents.

methodsWe combined the murine inferior vena cava stenosis model of deep vein thrombosis with the lipopolysaccharide model of endotoxemia. We also performed a proof-of-concept study of imaging mass cytometry to assess the feasibility of this approach in analyzing the structural composition of thrombi.

resultsWe found that lipopolysaccharide-treated mice had significantly higher incidences of venous thrombosis, an effect that was mitigated when VWF was inhibited using inhibitory αVWF antibodies. Our detailed structural analysis also showed that most thrombus components are localized in the white thrombus regardless of endotoxemia. Moreover, although endotoxemia modulated the relative representation and interactions of VWF with other thrombus constituents, the scaffolding network, comprised VWF, fibrin, and neutrophil extracellular traps, remained largely unaffected.

conclusionsWe observe a key role for VWF in the pathogenesis of inflammation-associated venous thrombosis while providing a more comprehensive insight into the molecular interactions that constitute the architecture of venous thrombi.

Indexed as

EndotoxemiaThrombosisVenous ThrombosisAnimalsLipopolysaccharidesMicevon Willebrand FactorLipopolysaccharidesvon Willebrand Factoranimal modelsimage cytometrythromboinflammationvenous thrombosisvon Willebrand factor

Identifiers

PMID36696220
PMCPMC11552101
OpenAlexW4317940533

What OpenQuestion holds

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LicenceTDM
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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.