ArticleInternational journal of molecular sciences2020
Characterization of Procoagulant COAT Platelets in Patients with Glanzmann Thrombasthenia.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Murine thrombus organization limits access to high platelet activation states while supporting platelet recruitment.Blood vessels, thrombosis & hemostasis · 2026Article
- Impact of recalcification on procoagulant collagen-and-thrombin-activated (COAT) platelet generation in platelet-rich plasma samples with low platelet counts.Research and practice in thrombosis and haemostasis · 2026Article
- Depletion of all platelet integrins impacts hemostasis, thrombosis, and tumor metastasis.iScience · 2025Article
- Flow cytometry immunophenotyping of healthy platelets and hospitalized patients with suspected platelet dysfunction: Challenges for establishing a cutoff value.Hematology, transfusion and cell therapy · 2024Article
- A thrombus is formed by a gradient of platelet activation and procoagulant endothelium.Research and practice in thrombosis and haemostasis · 2023Article
- Mechanisms Underlying Dichotomous Procoagulant COAT Platelet Generation-A Conceptual Review Summarizing Current Knowledge.International journal of molecular sciences · 2022Review
- Thrombocytopathies: Not Just Aggregation Defects-The Clinical Relevance of Procoagulant Platelets.Journal of clinical medicine · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Patients affected by the rare Glanzmann thrombasthenia (GT) suffer from defective or low levels of the platelet-associated glycoprotein (GP) IIb/IIIa, which acts as a fibrinogen receptor, and have therefore an impaired ability to aggregate platelets. Because the procoagulant activity is a dichotomous facet of platelet activation, diverging from the aggregation endpoint, we were interested in characterizing the ability to generate procoagulant platelets in GT patients. Therefore, we investigated, by flow cytometry analysis, platelet functions in three GT patients as well as their ability to generate procoagulant collagen-and-thrombin (COAT) platelets upon combined activation with convulxin-plus-thrombin. In addition, we further characterized intracellular ion fluxes during the procoagulant response, using specific probes to monitor by flow cytometry kinetics of cytosolic calcium, sodium, and potassium ion fluxes. GT patients generated higher percentages of procoagulant COAT platelets compared to healthy donors. Moreover, they were able to mobilize higher levels of cytosolic calcium following convulxin-plus-thrombin activation, which is congruent with the greater procoagulant activity. Further investigations will dissect the role of GPIIb/IIIa outside-in signalling possibly implicated in the regulation of platelet procoagulant activity.
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Registered trials
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