ArticleThe Journal of clinical investigation1994
Absence of ligands bound to glycoprotein IIB-IIIA on the exposed surface of a thrombus may limit thrombus growth in flowing blood.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
Who cites it
3 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Mechanism of platelet adhesion to von Willebrand factor and microparticle formation under high shear stress.Blood · 2006Article
- New directions in anticoagulant and antiplatelet treatment.Heart (British Cardiac Society) · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We examined the distribution of glycoprotein IIb-IIIa (GPIIb-IIIa) and its ligands fibrinogen and von Willebrand factor (vWf) on platelets which had adhered under flow conditions. Immunoelectron microscopy was performed on whole mounts and frozen thin sections of adhering platelets. GPIIb-IIIa was homogeneously distributed on dendritic platelets and on interplatelet membranes of formed thrombi. Fibrinogen and vWf were predominantly associated with interplatelet membranes and membranes facing the substrate. On whole mounts, vWf appeared in clumps and linear arrays, representing the tangled or extended forms of the multimeric molecule. From semiquantitative analysis, it appeared that fibrinogen and vWf were, respectively, nine- and fourfold higher on interplatelet membranes than on surface membranes facing the blood stream, while GPIIb-IIIa was evenly distributed over all platelet plasma membranes. Ligand-induced binding sites (LIBS) of GPIIb-IIIa, as measured with conformation specific monoclonal antibodies RUU 2.41 and LIBS-1, were present on the surface of adhered platelets and thrombi. A redistribution of LIBS-positive forms of GPIIb-IIIa towards interplatelet membranes was not observed. Our data support the hypothesis that, under flow conditions, ligands have first bound to activated GPIIb-IIIa but this binding is reversed on the upper surface of adhering platelets. This relative absence of ligands on the exposed surface of thrombi may play a role in limiting their size.
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