Endothelial cell source dictates the expression and release of fibrinolytic markers in a proinflammatory environment
Year: 2025
Type: article
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: ) shear stress. ECs were stimulated with thrombin, interleukin 6, or tumor necrosis factor (TNF)-α for 24 hours. The expression of coagulation and fibrinolytic proteins was quantified by quantitative polymerase chain reaction and secreted proteins via ELISA or activity assay. Plasma clot lysis on ECs ± 300 pM tissue-type plasminogen activator (tPA) was monitored at 405 nm. Results: < .05) respectively, but were normalized by neutralizing PAI-1. TNF-α stimulation of HCAECs prolonged clot lysis in a PAI-1-dependent manner. 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.
Institution: University of Aberdeen
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,250
OpenAlex ID: W4411196914