Evidence map›Paper›PMID 23753027›Full record

ArticleHaematologica2013

Platelet interaction with von Willebrand factor is enhanced by shear-induced clustering of glycoprotein Ibα.

Eelo Gitz, Charlotte D Koopman, Alèkos Giannas, Cornelis A Koekman, Dave J van den Heuvel, Hans Deckmyn, Jan-Willem N Akkerman, Hans C Gerritsen, Rolf T Urbanus

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  11. Akt-mediated platelet apoptosis and its therapeutic implications in immune thrombocytopenia.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. Temperature effects on the activity, shape, and storage of platelets from 13-lined ground squirrels.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2017
    Article
  14. Flow-Induced Damage to Blood Cells in Aortic Valve Stenosis.Annals of biomedical engineering · 2016
    Article
  15. Article
  16. Article
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  18. Review
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

9 authors at 3 institutions in 2 countries.

Eelo Gitzr.t.urbanus@umcutrecht.nl.
Charlotte D Koopman
Alèkos Giannas
Cornelis A Koekman
Dave J van den Heuvel
Hans Deckmyn
Jan-Willem N Akkerman
Hans C Gerritsen
Rolf T Urbanus
University Medical Center Utrecht · NLUtrecht University · NLResearch Institute for Chromatography · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Initial platelet arrest at the exposed arterial vessel wall is mediated through glycoprotein Ibα binding to the A1 domain of von Willebrand factor. This interaction occurs at sites of elevated shear force, and strengthens upon increasing hydrodynamic drag. The increased interaction requires shear-dependent exposure of the von Willebrand factor A1 domain, but the contribution of glycoprotein Ibα remains ill defined. We have previously found that glycoprotein Ibα forms clusters upon platelet cooling and hypothesized that such a property enhances the interaction with von Willebrand factor under physiological conditions. We analyzed the distribution of glycoprotein Ibα with Förster resonance energy transfer using time-gated fluorescence lifetime imaging microscopy. Perfusion at a shear rate of 1,600 s(-1) induced glycoprotein Ibα clusters on platelets adhered to von Willebrand factor, while clustering did not require von Willebrand factor contact at 10,000 s(-1). Shear-induced clustering was reversible, not accompanied by granule release or αIIbβ3 activation and improved glycoprotein Ibα-dependent platelet interaction with von Willebrand factor. Clustering required glycoprotein Ibα translocation to lipid rafts and critically depended on arachidonic acid-mediated binding of 14-3-3ζ to its cytoplasmic tail. This newly identified mechanism emphasizes the ability of platelets to respond to mechanical force and provides new insights into how changes in hemodynamics influence arterial thrombus formation.

Indexed as

Blood PlateletsCell AdhesionCluster AnalysisHumansPlatelet Glycoprotein GPIb-IX ComplexProtein BindingRandom AllocationShear Strengthvon Willebrand FactorPlatelet Glycoprotein GPIb-IX Complexvon Willebrand Factor

Identifiers

PMID23753027
PMCPMC3815184
OpenAlexW2112989578

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.