Shear stress-induced binding of von willebrand factor to platelets

Κωνσταντόπουλος, Κωνσταντίνος; Chow, T.W.; Turner, Nancy A.; Hellums, J. D.; Moake, Joel L.

doi:10.1016/s0006-355x(97)00004-8

Cited by 36 publications

(17 citation statements)

References 31 publications

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“…High shear forces enhance platelet-induced hemostasis at sites of vessel wall injury (57). GP Ib-vWF complexes play an important role in platelet adhesion to the vascular wall (58,59). Given the fact that GP Ib has separate binding sites for vWF and thrombin, it is possible that the binding of one ligand will synergistically facilitate the binding of the other ligand to the same GP Ib molecule or to a different GP Ib molecule.…”

Section: Resultsmentioning

confidence: 99%

Unique Pathway of Thrombin-induced Platelet Aggregation Mediated by Glycoprotein Ib

Soslau

Class

Morgan

et al. 2001

Journal of Biological Chemistry

159

155

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Section: Resultsmentioning

confidence: 99%

Unique Pathway of Thrombin-induced Platelet Aggregation Mediated by Glycoprotein Ib

Soslau

Class

Morgan

et al. 2001

Journal of Biological Chemistry

159

155

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“…Ten thousand events were acquired and analyzed for FITC fluorescence, considered as an index of binding of the reporter anti-human FITC antibody. Results were expressed as the percentage of vWF-positive platelets above the threshold fluorescence of the control platelet samples (Konstantopoulos et al 1997). …”

Section: Ristocetin-induced Platelet Aggregationmentioning

confidence: 99%

Intense exercise increases shear-induced platelet aggregation in men through enhancement of von Willbrand factor binding, glycoprotein IIb/IIIa activation, and P-selectin expression on platelets

Wang

2004

European Journal of Applied Physiology

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Vigorous exercise transiently enhances the risk of primary cardiac arrest. Shear-induced platelet aggregation (SIPA) is an important mechanism in arterial thrombogenesis. This study investigates whether intense exercise affects SIPA, and elucidates mechanisms that underlie SIPA. Eighteen sedentary healthy men engaged in intense exercise (about 80% of maximal oxygen consumption) for 40 min on a bicycle ergometer. Platelet aggregation, binding of von Willebrand factor (vWF) to platelets, and activation of glycoprotein (GP) IIb/IIIa and expression of P-selectin on platelets induced by shear stress were analyzed both before and immediately after exercise. Analytical results demonstrated that: (1). the levels of plasma vWF antigen and activity were enhanced after intense exercise, (2). intense exercise increased either shear- or ristocetin-induced platelet aggregation and was accompanied by an increase in vWF binding to platelets and vWF-mediated GP IIb/IIIa activation at high shear flow, and (3). shear-induced P-selectin expression in the absence or the presence of exogenous vWF was enhanced by intense exercise. Therefore, we conclude that intense exercise promotes the extent of SIPA, possibly by enhancing the ability of vWF to bind to platelets and the subsequent activation of GP IIb/IIIa complexes, as well as the expression of P-selectin in response to shear stress, which in turn may augment the risk of vascular thrombosis.

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“…As maximum shear rates in the current work ranged from about 1800–3100 s −1 , platelets were assumed to adhere to von Willebrand factor immobilized on the subendothelium through glycoproteins GPIb or GPIIb-IIIa, and to aggregate with each other through bridging of GPIb or GPIIb-IIIa by plasma von Willebrand factor (Ikeda et al, 1991; Kroll et al, 1996; Konstantopoulos et al, 1997; Shankaran et al, 2003). At low shear rates, RBCs aggregate with each other, while at high shear rates these aggregates break up.…”

Section: Methodsmentioning

confidence: 99%

“…Hence, the scaling factor was chosen to be f = 1.042. The critical shear stress was chosen based on in vitro experiments with whole blood and platelet rich plasma, which showed that shear-induced platelet activation and aggregation occurred at shear stresses that ranged from 15 to 30 dyn cm −2 (Chow et al, 1992; Konstantopoulos et al, 1995, 1997; Shankaran et al, 2003). Although some of these experiments also showed large increases in platelet activation and aggregation as shear stresses surpassed 75–140 dyn cm −2 , our critical shear stress was chosen to illustrate trends in the early stage of thrombus formation with respect to changes in shear stress due to tortuosity.…”

Section: Methodsmentioning

confidence: 99%

Effect of Red Blood Cells on Platelet Activation and Thrombus Formation in Tortuous Arterioles

Chesnutt

Han

2013

Front. Bioeng. Biotechnol.

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Thrombosis is a major contributor to cardiovascular disease, which can lead to myocardial infarction and stroke. Thrombosis may form in tortuous microvessels, which are often seen throughout the human body, but the microscale mechanisms and processes are not well understood. In straight vessels, the presence of red blood cells (RBCs) is known to push platelets toward walls, which may affect platelet aggregation and thrombus formation. However in tortuous vessels, the effects of RBC interactions with platelets in thrombosis are largely unknown. Accordingly, the objective of this work was to determine the physical effects of RBCs, platelet size, and vessel tortuosity on platelet activation and thrombus formation in tortuous arterioles. A discrete element computational model was used to simulate the transport, collision, adhesion, aggregation, and shear-induced platelet activation of hundreds of individual platelets and RBCs in thrombus formation in tortuous arterioles. Results showed that high shear stress near the inner sides of curved arteriole walls activated platelets to initiate thrombosis. RBCs initially promoted platelet activation, but then collisions of RBCs with mural thrombi reduced the amount of mural thrombus and the size of emboli. In the absence of RBCs, mural thrombus mass was smaller in a highly tortuous arteriole compared to a less tortuous arteriole. In the presence of RBCs however, mural thrombus mass was larger in the highly tortuous arteriole compared to the less tortuous arteriole. As well, smaller platelet size yielded less mural thrombus mass and smaller emboli, either with or without RBCs. This study shed light on microscopic interactions of RBCs and platelets in tortuous microvessels, which have implications in various pathologies associated with thrombosis and bleeding.

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Shear stress-induced binding of von willebrand factor to platelets

Cited by 36 publications

References 31 publications

Unique Pathway of Thrombin-induced Platelet Aggregation Mediated by Glycoprotein Ib

Unique Pathway of Thrombin-induced Platelet Aggregation Mediated by Glycoprotein Ib

Intense exercise increases shear-induced platelet aggregation in men through enhancement of von Willbrand factor binding, glycoprotein IIb/IIIa activation, and P-selectin expression on platelets

Effect of Red Blood Cells on Platelet Activation and Thrombus Formation in Tortuous Arterioles

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