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      Platelets Drive Thrombus Propagation in a Hematocrit and Glycoprotein VI–Dependent Manner in an In Vitro Venous Thrombosis Model

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          Abstract

          The objective of this study was to measure the role of platelets and red blood cells on thrombus propagation in an in vitro model of venous valvular stasis.

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          Clot contraction: compression of erythrocytes into tightly packed polyhedra and redistribution of platelets and fibrin.

          Douglas Cines, Tatiana Lebedeva, Chandrasekaran Nagaswami … (2014)
          Contraction of blood clots is necessary for hemostasis and wound healing and to restore flow past obstructive thrombi, but little is known about the structure of contracted clots or the role of erythrocytes in contraction. We found that contracted blood clots develop a remarkable structure, with a meshwork of fibrin and platelet aggregates on the exterior of the clot and a close-packed, tessellated array of compressed polyhedral erythrocytes within. The same results were obtained after initiation of clotting with various activators and also with clots from reconstituted human blood and mouse blood. Such close-packed arrays of polyhedral erythrocytes, or polyhedrocytes, were also observed in human arterial thrombi taken from patients. The mechanical nature of this shape change was confirmed by polyhedrocyte formation from the forces of centrifugation of blood without clotting. Platelets (with their cytoskeletal motility proteins) and fibrin(ogen) (as the substrate bridging platelets for contraction) are required to generate the forces necessary to segregate platelets/fibrin from erythrocytes and to compress erythrocytes into a tightly packed array. These results demonstrate how contracted clots form an impermeable barrier important for hemostasis and wound healing and help explain how fibrinolysis is greatly retarded as clots contract.
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            New insights into the mechanisms of venous thrombosis.

            Nigel Mackman (2012)
            Venous thrombosis is a leading cause of morbidity and mortality in industrialized countries, especially in the elderly. Many risk factors have been identified for venous thrombosis that alter blood flow, activate the endothelium, and increase blood coagulation. However, the precise mechanisms that trigger clotting in large veins have not been fully elucidated. The most common site for initiation of the thrombus appears to be the valve pocket sinus, due to its tendency to become hypoxic. Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis. Understanding the mechanisms of venous thrombosis may lead to the development of new treatments.
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              Platelet glycoprotein VI binds to polymerized fibrin and promotes thrombin generation.

              Elmina Mammadova-Bach, Véronique Ollivier, Stéphane Loyau … (2015)
              Fibrin, the coagulation end product, consolidates the platelet plug at sites of vascular injury and supports the recruitment of circulating platelets. In addition to integrin αIIbβ3, another as-yet-unidentified receptor is thought to mediate platelet interaction with fibrin. Platelet glycoprotein VI (GPVI) interacts with collagen and several other adhesive macromolecules. We evaluated the hypothesis that GPVI could be a functional platelet receptor for fibrin. Calibrated thrombin assays using platelet-rich plasma (PRP) showed that tissue factor-triggered thrombin generation was impaired in GPVI-deficient patients and reduced by the anti-GPVI Fab 9O12. Assays on reconstituted PRP and PRP from fibrinogen-deficient patients revealed a fibrinogen-dependent enhancement of thrombin generation, which relied on functional GPVI. The effect of GPVI was found to depend on fibrin polymerization. A binding assay showed a specific interaction between GPVI-Fc and fibrin, inhibited by the Fab 9O12. This Fab also reduced platelet adhesion to fibrin at low (300 s(-1)) and high (1500 s(-1)) wall shear rates. Platelets adherent to fibrin displayed shape change, exposure of procoagulant phospholipids, and the formation of small clots. When hirudinated blood was perfused at 1500 s(-1) over preformed fibrin-rich clots, the Fab 9O12 decreased the recruitment of platelets by up to 85%. This study identifies GPVI as a platelet receptor for polymerized fibrin with 2 major functions: (1) amplification of thrombin generation and (2) recruitment of circulating platelets to clots. These so-far-unrecognized properties of GPVI confer on it a key role in thrombus growth and stabilization.
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                Author and article information

                Journal
                Title: Arteriosclerosis, Thrombosis, and Vascular Biology
                Abbreviated Title: Arterioscler Thromb Vasc Biol.
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 1079-5642
                ISSN (Electronic): 1524-4636
                Publication date Created: May 2018
                Publication date (Print): May 2018
                Volume: 38
                Issue: 5
                Pages: 1052-1062
                Affiliations
                [1 ]From the Chemical and Biological Engineering Department, Colorado School of Mines, Golden (M.L., R.M.S., P.J.K., A.M.W., J.R.S., K.B.N.)
                [2 ]Laboratory of Vascular Translational Science, UMR_S1148, INSERM, University Paris Diderot, France (M.J.-P.)
                [3 ]Department of Pediatrics, University of Colorado, Aurora (K.B.N.).
                Article
                DOI: 10.1161/ATVBAHA.118.310731
                PMC ID: 5920765
                PubMed ID: 29472230
                SO-VID: d42b5825-cd3c-44f1-97a7-fc0df561f2a3
                Copyright © © 2018
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