ArticleJournal of thrombosis and haemostasis : JTH2020
Phagocytosis by endothelial cells inhibits procoagulant activity of platelets of essential thrombocythemia in vitro.
Article in Journal of thrombosis and haemostasis : JTH, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
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- Ferroptosis of Endothelial Cells Triggered by Erythrophagocytosis Contributes to Thrombogenesis in Uremia.Thrombosis and haemostasis · 2023Article
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- Mechanisms of platelet activation in cancer-associated thrombosis: a focus on myeloproliferative neoplasms.Frontiers in cell and developmental biology · 2023Review
- Immune Function of Endothelial Cells: Evolutionary Aspects, Molecular Biology and Role in Atherogenesis.International journal of molecular sciences · 2022Review
- Strategies for Delivering Nanoparticles across Tumor Blood Vessels.Advanced functional materials · 2021Article
- Horizontal MicroRNA Transfer by Platelets - Evidence and Implications.Frontiers in physiology · 2021Review
- Non-Alloimmune Mechanisms of Thrombocytopenia and Refractoriness to Platelet Transfusion.Transfusion medicine reviews · 2020Review
- Phagocytosis by endothelial cells inhibits procoagulant activity of platelets of essential thrombocythemia in vitro.Journal of thrombosis and haemostasis : JTH · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEssential thrombocythemia (ET) is characterized by thrombocytosis with increased platelet number and persistent activation. The mechanisms of thrombosis and the fate of these platelets are not clear. The aim of the present study is to explore the phagocytosis of platelets of ET patients by endothelial cells (ECs) in vitro and its relevance to the procoagulant activity (PCA).
methodsPhosphatidylserine (PS) exposure on platelets was detected by flow cytometry. Phagocytosis of the platelets by ECs was performed using flow cytometry, confocal microscopy, and electron microscopy. The PCA of platelets was evaluated by coagulation time and purified coagulation complex assays.
resultsThe PS exposure on platelets in ET patients is higher than that in healthy controls. The PS-exposed platelets are highly procoagulant and lactadherin reduced 80% of the PCA by blockade of PS. When cocultured, the platelets of ET patients were sequestered by ECs in a time-dependent fashion. Lactadherin enhanced phagocytosis by bridging the PS on activated platelets and the integrin αvβ3 on ECs, and P-selectin played at least a partial role in this process. Furthermore, factor Xa and prothrombinase activity of PS-exposed platelets were decreased after incubation with ECs.
conclusionOur results suggest that phagocytic clearance of platelets by ECs occurs in ET patients, thus representing a novel mechanism to remove activated platelets from the circulation; lactadherin and phagocytosis could cooperatively limit the thrombophilia in ET patients.
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