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Platelets adhere to thrombin-treated endothelial cells in vitro.
J E Kaplan1, D G Moon, L K Weston
1Department of Physiology, Albany Medical College of Union University 12208.
The American Journal of Physiology
|August 1, 1989
Summary
Thrombin binding to endothelial cells activates platelets, promoting their adherence. This interaction involves retained active thrombin on endothelial cells, leading to platelet activation and aggregation on the vessel wall.
Area of Science:
- Cardiovascular Biology
- Hemostasis and Thrombosis
- Endothelial Cell Biology
Background:
- Thrombin plays a critical role in hemostasis and thrombosis.
- Understanding thrombin's interaction with endothelial cells is crucial for elucidating platelet-endothelial cell dynamics.
Purpose of the Study:
- To investigate the mechanism by which thrombin interaction with vascular endothelial cells promotes platelet activation and adherence.
- To determine if active thrombin is retained by endothelial cells and remains functional.
Main Methods:
- Endothelial cell monolayers and aortic segments were pretreated with alpha-thrombin.
- Platelet attachment assays were performed after removal of fluid-phase thrombin.
- Active site inhibitors and radiolabeled serotonin release assays were used to assess thrombin activity and platelet activation.
- Divalent cation dependence was evaluated.
Main Results:
- Pretreatment of endothelium with alpha-thrombin led to platelet attachment even after thrombin removal.
- This adherence was mediated by retained active thrombin on endothelial cells via a receptor-dependent mechanism.
- Platelets exhibited activation and aggregation on thrombin-pretreated endothelium.
- Adherence was dependent on divalent cations.
Conclusions:
- Endothelial cells can bind and retain active alpha-thrombin.
- Retained active thrombin on endothelial cells promotes platelet activation and adherence.
- This mechanism contributes to thrombus formation on the vascular wall.