ArticleResearch and practice in thrombosis and haemostasis2025
A cell-based model to study mechanisms of endothelial-dependent thrombin generation in response to inflammation and its modulation by hydroxychloroquine.
Article in Research and practice in thrombosis and haemostasis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Inflammatory Manifestations, Therapeutic Interventions, and Cancer Risk in Psoriasis: Current Epidemiological and Mechanistic Evidence.International journal of molecular sciences · 2026Review
- Review
- Endothelial cell source dictates the expression and release of fibrinolytic markers in a proinflammatory environment.Research and practice in thrombosis and haemostasis · 2025Article
- Unresolved issues in the diagnosis and management of thrombotic antiphospholipid syndrome.Research and practice in thrombosis and haemostasis · 2025Article
- Smart Thrombosis Care: The Rise of Closed-Loop Diagnosis-to-Treatment Nano Systems.International journal of nanomedicine · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
Background: Inflammation is a driver of thrombosis, but the phenomenon of thromboinflammation has been defined only recently, bringing together the multiple pathways involved. Objectives: To develop a model for thrombin generation (TG) on the surface of human endothelial cells (ECs) to assess pro/antithrombotic properties in response to inflammation. Furthermore, to elucidate the mechanisms of TG regulation and its modulation by immunomodulatory therapies. Methods: Cytokine-induced (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and interferon-γ) effects on ECs isolated from umbilical veins or human aortic tissue were assessed using calibrated automated thrombography in platelet-poor plasma. The expression of key coagulant and inflammatory regulators was measured at the mRNA level. Tissue factor (TF) protein levels were further assessed by flow cytometry. Results: Endothelial stimulation with TNF-α or IL-1β caused ECs to trigger TG without the addition of exogenous TF, with higher TG observed after 6 hours of stimulation than 24 hours. IL-1β induced higher peak thrombin (170 ± 5.9 nM vs 115 ± 4.9 nM), endogenous thrombin potential (1632 ± 35 nM ∗ min vs 1370 ± 23 nM ∗ min) presented as mean ± SD, and TF expression (∼2.8-fold higher) compared with TNF-α at 6 hours. Interferon-γ stimulation failed to induce TG and TF expression. The immunomodulatory drug, hydroxychloroquine, reduced cytokine-induced TG and downregulated TF expression. Conclusion: We provide detailed optimization of a robust
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