ArticleResearch and practice in thrombosis and haemostasis2025
Endothelial cell source dictates the expression and release of fibrinolytic markers in a proinflammatory environment.
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 3 papers.
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Who cites it
3 citing papers in PubMed.
- Autoimmune-associated thrombosis: mechanisms, population burden, and prevention strategies.The Lancet regional health. Europe · 2026Review
- Endothelial Cell Activation by SARS-CoV-2 Spike Protein and Its RBD: Central Player of the Immunothrobotic Response in COVID-19.Current issues in molecular biology · 2026Article
- Molecular biomarkers in dialysis-related thrombosis and anticoagulation monitoring: thrombin-antithrombin complex, plasmin-α2-antiplasmin complex, soluble thrombomodulin, tPA/PAI-1/tPAIC, and Anti-Xa.Frontiers in medicine · 2026Review
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Authors and funding
3 authors.
Funding
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Abstract
Background: Endothelial cells (ECs) provide a surface for molecular interactions, secreting various factors that govern hemostasis. Inflammatory cytokines can perturb the vascular microenvironment, potentially causing endothelial dysfunction and dysregulation of hemostasis. Objectives: To examine the fibrinolytic balance of ECs from different vascular beds and their response to proinflammatory stimuli. Methods: Primary human umbilical vein ECs (HUVECs), human coronary artery ECs (HCAECs), and immortalized EA.hy926 cells were cultured under venous (2.5 dyne/cm Results: Basal secretion of C-reactive protein, urokinase plasminogen activator (uPA), and plasminogen activator inhibitor-1 (PAI-1) was higher in HCAECs than in HUVECs, but tPA was similar in both. TNF-α stimulation of HCAECs increased secretion of tPA, uPA, and PAI-1. Levels of tPA/PAI-1 and uPA/PAI-1 were higher in media, as was free-active PAI-1. In contrast, stimulation of HUVECs did not significantly alter gene/protein levels. HCAECs and HUVECs delayed clot lysis relative to no-cell controls by 11 ± 8 minutes ( Conclusion: HCAECs respond more potently to a proinflammatory environment than HUVECs, altering expression of fibrinolytic proteins and promoting a hypofibrinolytic response. These data highlight HCAECs as a model of coronary vasculature with potential for screening novel antithrombotic strategies.
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