Related Experiment Video
Updated: Jul 21, 2026

A Novel In vitro Model for Studying the Interactions Between Human Whole Blood and Endothelium
Published on: November 21, 2014
Binding of thrombin to cultured human endothelial cells. Nonequilibrium aspects
Abstract:
The long-term incubation of 125I-thrombin with cultured human endothelial cells is studied and compared to the previously described rapid equilibrium binding in this system (Awbrey, B. J., Hoak, J. C., and Owen, W. G. (1979) J. Biol. Chem. 254, 4092-4095). Following rapid initial binding of thrombin, a much slower association of thrombin with endothelium is seen. As opposed to equilibrium binding, this process is 1) irreversible, 2) active-site specific, and 3) associated with covalent linkage to an Mr 30,000 protein. In addition this nonequilibrium binding appears unrelated to high-affinity equilibrium binding since blocking the high-affinity binding sites with diisopropylphosphoryl thrombin has no effect on nonequilibrium binding. The physiological role of this process is unknown.
More Related Videos
09:38A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
Published on: February 14, 2017
09:19In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
Published on: May 24, 2020
Related Concept Videos
Intracellular Signaling Affects Focal Adhesions
Some...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Clot Retraction and Fibrinolysis