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Updated: Jul 29, 2026

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
11:18

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

Published on: April 2, 2013

Evidence that activation of platelets and endothelium by thrombin involves distinct sites of interaction. Studies

R A Henriksen, A F Brotherton

    The Journal of Biological Chemistry
    |November 25, 1983
    PubMed

    Previous results indicate extensive similarity of the active site regions of thrombin (EC 3.4.21.5) and Thrombin Quick, a congenital dysthrombin. A binding defect of Thrombin Quick toward fibrinogen is indicated by an increased KI when fibrinogen is present as a competitive inhibitor in the hydrolysis of tosyl-Gly-Pro-Arg-p-nitroanilide. In the present study, Thrombin Quick I is shown to have an activity of 1.3 and 34%, respectively, toward fibrinogen and prothrombin. Like the activity observed in prothrombin hydrolysis, Thrombin Quick I was 30% as effective as thrombin in stimulating release of thromboxane from platelets. Thrombin Quick was 1.7 and 2.4%, as effective as thrombin in stimulating platelet aggregation and prostacyclin production, respectively. Based on the activity of Thrombin Quick I in the reactions investigated, it is concluded that 1) the three cellular responses studied are initiated by proteolytic action of thrombin, 2) thrombin stimulation of aggregation and thromboxane release from platelets occurs via two different receptors, 3) the thrombin cellular interaction resulting in platelet aggregation and prostacyclin release must involve the thrombin active site as well as a secondary binding site required for optimal interaction with fibrinogen, and 4) the release of thromboxane from platelets does not involve the interaction of thrombin at the extrinsic binding site.

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