ArticleJournal of thrombosis and haemostasis : JTH2009
Endothelial cell specific adhesion molecule (ESAM) localizes to platelet-platelet contacts and regulates thrombus formation in vivo.
Article in Journal of thrombosis and haemostasis : JTH, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed, 69 citations in OpenAlex.
- Relationship between biomarkers and subsequent bleeding risk in ST-segment elevation myocardial infarction patients treated with paclitaxel-eluting stents: a HORIZONS-AMI substudy.Journal of thrombosis and thrombolysis · 2013Trial
- Niacin and biosynthesis of PGD₂by platelet COX-1 in mice and humans.The Journal of clinical investigation · 2012 · on this mapTrial
- ZO-2 seals the deal for platelet tight junctions.Research and practice in thrombosis and haemostasis · 2025Article
- Sex Differences in Thrombin Generation in Patients with Acute Ischemic Stroke.Translational stroke research · 2025Article
- Characteristics of cell adhesion molecules expression and environmental adaptation in yak lung tissue.Scientific reports · 2025Article
- Formation of tight junction-like structures of zonula occludens 2 in platelet-platelet interaction.Research and practice in thrombosis and haemostasis · 2025Article
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- 3D Visualization of Human Blood Vascular Networks Using Single-Domain Antibodies Directed against Endothelial Cell-Selective Adhesion Molecule (ESAM).International journal of molecular sciences · 2022Article
- Src family kinases inhibition by dasatinib blocks initial and subsequent platelet deposition on collagen under flow, but lacks efficacy with thrombin generation.Thrombosis research · 2020Article
- Platelet integrin αIIbβ3: signal transduction, regulation, and its therapeutic targeting.Journal of hematology & oncology · 2019Review
- Functional Genomics for the Identification of Modulators of Platelet-Dependent Thrombus Formation.TH open : companion journal to thrombosis and haemostasis · 2018Review
- Negative regulators of platelet activation and adhesion.Journal of thrombosis and haemostasis : JTH · 2018Review
- Proteomics identification of radiation-induced changes of membrane proteins in the rat model of arteriovenous malformation in pursuit of targets for brain AVM molecular therapy.Clinical proteomics · 2018Article
- Role of the PDZ-scaffold protein NHERF1/EBP50 in cancer biology: from signaling regulation to clinical relevance.Oncogene · 2017Review
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- Platelet signaling: a complex interplay between inhibitory and activatory networks.Journal of thrombosis and haemostasis : JTH · 2016Review
- Soluble endothelial cell selective adhesion molecule and cardiovascular outcomes in patients with stable coronary disease: A report from the Heart and Soul Study.Atherosclerosis · 2015Article
- EphB2 regulates contact-dependent and contact-independent signaling to control platelet function.Blood · 2015Article
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Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIn resting platelets, endothelial cell specific adhesion molecule (ESAM) is located in alpha granules, increasing its cell surface expression following platelet activation. However, the function of ESAM on platelets is unknown.
objectiveTo determine whether ESAM has a role in thrombus formation. METHODS AND
resultsWe found that following platelet activation ESAM localizes to the junctions between adjacent platelets, suggesting a role for this protein in contact-dependent events that regulate thrombus formation. To test this hypothesis we examined the effect of ESAM deletion on platelet function. In vivo, ESAM(-/-) mice achieved more stable hemostasis than wild-type mice following tail transection, and developed larger thrombi following laser injury of cremaster muscle arterioles. In vitro, ESAM(-/-) platelets aggregated at lower concentrations of G protein-dependent agonists than wild-type platelets, and were more resistant to disaggregation. In contrast, agonist-induced calcium mobilization, alpha(IIb)beta(3) activation, alpha-granule secretion and platelet spreading, were normal in ESAM-deficient platelets. To understand the molecular mechanism by which ESAM regulates platelet activity, we utilized a PDZ domain array to identify the scaffold protein NHERF-1 as an ESAM binding protein, and further demonstrated that it associates with ESAM in both resting and activated platelets.
conclusionsThese findings support a model in which ESAM localizes to platelet contacts following platelet activation in order to limit thrombus growth and stability so that the optimal hemostatic response occurs following vascular injury.
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Registered trials
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.