Evidence map›Paper›PMID 21368290›Full record

ArticleBlood2011

Heparin promotes platelet responsiveness by potentiating αIIbβ3-mediated outside-in signaling.

Cunji Gao, Brian Boylan, Juan Fang, David A Wilcox, Debra K Newman, Peter J Newman

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Platelets are dominant contributors to hypercoagulability after injury.The journal of trauma and acute care surgery · 2013
    Trial
  4. Trial
  5. Review
  6. Impact of Pre-PCI Activated Clotting Time on Outcomes of Bivalirudin Versus Heparin During Primary PCI.Journal of the Society for Cardiovascular Angiography & Interventions · 2025
    Article
  7. Article
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  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
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  19. Article
  20. mTOR regulates GPVI-mediated platelet activation.Journal of translational medicine · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Cunji GaoBlood Research Institute, Medical College of Wisconsin, Milwaukee, WI, USA. cunji.gao@bcw.edu
Brian Boylan
Juan Fang
David A Wilcox
Debra K Newman
Peter J Newman
Versiti Blood Center of Wisconsin · USMedical College of Wisconsin · USPediatrics and Genetics · US

Funding

Transgenic/Knockout CoreP01HL044612 · NHLBI · VERSITI WISCONSIN, INC. · PI NEWMAN, PETER J · 1990 to 2015
$33.4M
NHLBI NIH HHS HL-44612NHLBI NIH HHS P01 HL044612
6 · The paper itself

Abstract

Unfractionated heparin (UFH) is a widely used anticoagulant that has long been known to potentiate platelet responses to subthreshold doses of platelet agonists. UFH has been reported to bind and induce modest conformational changes in the major platelet integrin, αIIbβ3, and induce minor changes in platelet morphology. The mechanism by which UFH elicits these platelet-activating effects, however, is not well understood. We found that both human and murine platelets exposed to UFH, either in solution or immobilized onto artificial surfaces, underwent biochemical and morphologic changes indicative of a potentiated state, including phosphorylation of key cytosolic signaling molecules and cytoskeletal changes leading to cell spreading. Low molecular weight heparin and the synthetic pentasaccharide, fondaparinux, had similar platelet-potentiating effects. Human or mouse platelets lacking functional integrin αIIbβ3 complexes and human platelets pretreated with the fibrinogen receptor antagonists eptifibatide or abciximab failed to become potentiated by heparin, demonstrating that heparin promotes platelet responsiveness via its ability to initiate αIIbβ3-mediated outside-in signaling. Taken together, these data provide novel insights into the mechanism by which platelets become activated after exposure to heparin and heparin-coated surfaces, and suggest that currently used glycoprotein IIb-IIIa inhibitors may be effective inhibitors of nonimmune forms of heparin-induced platelet activation.

Indexed as

AbciximabAdultAnimalsAntibodies, MonoclonalAnticoagulantsDrug SynergismEptifibatideFondaparinuxHeparinHumansImmunoglobulin Fab FragmentsIn Vitro TechniquesMiceModels, BiologicalPeptidesPlatelet ActivationAbciximabAntibodies, MonoclonalAnticoagulantsEptifibatideFondaparinuxHeparinImmunoglobulin Fab FragmentsPeptidesPlatelet Aggregation InhibitorsPlatelet Glycoprotein GPIIb-IIIa ComplexPolysaccharides

Identifiers

PMID21368290
PMCPMC3100701
OpenAlexW1988608065

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.