Interaction of platelets and purified collagens in a laminar flow model

Parsons, Thomas J.; Haycraft, D L; Hoak, John C.; Sage, Helene

doi:10.1016/0049-3848(86)90088-5

Cited by 33 publications

(8 citation statements)

References 21 publications

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“…Since platelet adhesion dominates at high shear, a static system measuring platelet adhesion may not be an accurate measure of EC thrombogenicity. For example, different results on the same EC have been observed using rocking versus laminar flow experimental systems [192]. Furthermore alterations in platelet adhesion with shear level have been seen in a capillary flow circuit using HUVEC cultured on fibronectin coated polyethylene [182].…”

Section: Dominant Factors Influencing Thrombogenicity Measurement-mentioning

confidence: 95%

The influence of biomaterials on endothelial cell thrombogenicity

2007

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Driven by tissue engineering and regenerative medicine, endothelial cells are being used in combination with biomaterials in a number of applications for the purpose of improving blood compatibility and host integration. Endothelialized vascular grafts are beginning to be used clinically with some success in some centers, while endothelial seeding is being explored as a means of creating a vasculature within engineered tissues. The underlying assumption of this strategy is that when cultured on artificial biomaterials, a confluent layer of endothelial cells maintain their nonthrombogenic phenotype. In this review the existing knowledge base of endothelial cell thrombogenicity cultured on a number of different biomaterials is summarized. The importance of selecting appropriate endpoint measures that are most reflective of overall surface thrombogenicity is the focus of this review. Endothelial cells inhibit thrombosis through three interconnected regulatory systems (1) the coagulation cascade (2) the cellular components of the blood such as leukocytes and platelets and (3) the complement cascade, and also through effects on fibrinolysis and vascular tone, the latter which influences blood flow. Thus, in order to demonstrate the thromobgenic benefit of seeding a biomaterial with EC, the conditions under which EC surfaces are more likely to exhibit lower thrombogenicity than unseeded biomaterial surfaces need to be consistent with the experimental context. The endpoints selected should be appropriate for the dominant thrombotic process that occurs under the given experimental conditions.

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Section: Dominant Factors Influencing Thrombogenicity Measurement-mentioning

confidence: 95%

The influence of biomaterials on endothelial cell thrombogenicity

2007

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“…Vitronectin and collagen type V were not studied because previous studies from our laboratory and others (55) have shown that these proteins are only adhesive under static conditions, but not in flow.…”

Section: Discussionmentioning

confidence: 99%

Increased platelet deposition on atherosclerotic coronary arteries.

Zanten¹,

Graaf²,

Slootweg³

et al. 1994

J. Clin. Invest.

159

106

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IntroductionA ruptured atherosclerotic plaque leads to exposure of deeper layers of the plaque to flowing blood and subsequently to thrombus formation. In contrast to the wealth of data on the occurrence of thrombi, little is known about the reasons why an atherosclerotic plaque is thrombogenic. One of the reasons is the relative inaccessibility of the atherosclerotic plaque. We have circumvented this problem by using 6-,gm cryostat cross sections of human coronary arteries. These sections were mounted on coverslips that were exposed to flowing blood in a rectangular perfusion chamber. In normal-appearing arteries, platelet deposition was seen on the luminal side of the intima and on the adventitia. In atherosclerotic arteries, strongly increased platelet deposition was seen on the connective tissue of specific parts of the atherosclerotic plaque. Despite the evident importance of this issue, few studies exist about the thrombogenicity of the atherosclerotic plaque. Coagulation tests with tissue extracts of atheromas (6, 7) and addition of atheroma suspension to blood in a rotating tilted closed plastic tube ("Chandler loop" model) (7-9) tended to show less thrombogenicity than expected (6,8,9). More recently histochemical studies showed that there is more tissue factor in an atherosclerotic plaque than in the normal vessel wall (10, 11). Perfusion studies with blood over hyperlipidemic rabbit atherosclerotic aortic subendothelium showed decreased platelet adhesion ( 12), whereas the injured artificially created neointima in rabbits was more thrombogenic than the injured normal intima ( 13 ). A problem of most studies is that the relevant deeper layers ofthe atherosclerotic plaque are relatively inaccessible to flowing blood. Artificial rupture of the atherosclerotic plaque in order to bring blood in contact with deeper layers has the disadvantage that it is difficult to evaluate the actual thrombogenicity because ofthe disturbed blood flow pattern. We have circumvented these problems by using cryostat cross sections of postmortem human coronary arteries. These cross sections were mounted on coverslips and anticoagulated blood was perfused over them in a rectangular perfusion chamber ( 14). These studies showed platelet deposition and thrombus formation particularly on the luminal side of the subendothelium and on the adventitia in normal vessels and strongly increased platelet deposition on the connective tissue of the atherosclerotic plaque. No platelet deposition was seen on the central lipid core of the atherosclerotic plaque.To study the cause of increased platelet deposition on the atherosclerotic plaque, perfusion studies over cross sections of atherosclerotic coronary arteries were combined with immunohistochemical studies and inhibition studies using antibodies and specific inhibitors. Methods SpecimensPostmortem coronary arteries from 25 patients with different causes of death and fresh coronary arteries from 11 patients who were undergoing cardiac transplantation were obtained from the Depart...

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“…Blood vessels contain different types of collagen; so far, collagen types I, III–VI, VIII and XII–XIV have been located in the vasculature [9,10]. Fibrillar collagen types I and III are major components of blood vessels, and type IV collagen is a basement membrane component.…”

Section: Introductionmentioning

confidence: 99%

A mechanism to safeguard platelet adhesion under high shear flow: von Willebrand factor–glycoprotein Ib and integrin α2β1–collagen interactions make complementary, collagen‐type‐specific contributions to adhesion

Moroi

Jung

2007

Journal of Thrombosis and Haemostasis

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To cite this article: Moroi M, Jung SM. A mechanism to safeguard platelet adhesion under high-shear flow: von Willebrand factor-glycoprotein Ib and integrin a 2 b 1 -collagen interactions make complementary, collagen-type-specific contributions to adhesion. J Thromb Haemost 2007; 5: 797-803.Summary. Background: Blood vessels contain different types of collagen, with types I and III being the major components of vascular collagen. Platelet adhesion under high shear stress has been suggested to depend on the binding of von Willebrand factor (VWF) to collagen. Objective: We analyzed the collagen type specificity for the interaction with VWF and high shear stress platelet adhesion. Methods: VWF binding to different types of immobilized collagen and effects of antibodies against glycoprotein Ib (gpIb) and integrin a 2 b 1 on platelet adhesion to type I and III collagens under high shear were analyzed. Results: VWF showed high-affinity, selective binding to human and bovine type III collagens, but weak or no affinity for types I, II, IV and V under static conditions. Anti-integrin a 2 b 1 markedly inhibited adhesion to type I collagen, but did not affect that to type III collagen. Anti-gpIb antibody significantly inhibited adhesion to type III collagen. Adding both antibodies abrogated the adhesion to either type I or III collagen. Conclusions: Both the gpIb-VWF interaction and the integrin a 2 b 1 -collagen interaction contribute to platelet adhesion to collagen under high shear stress, and integrin a II b 1 makes a greater contribution to adhesion to type I collagen because less VWF is bound to it.

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Interaction of platelets and purified collagens in a laminar flow model

Cited by 33 publications

References 21 publications

The influence of biomaterials on endothelial cell thrombogenicity

The influence of biomaterials on endothelial cell thrombogenicity

Increased platelet deposition on atherosclerotic coronary arteries.

A mechanism to safeguard platelet adhesion under high shear flow: von Willebrand factor–glycoprotein Ib and integrin α2β1–collagen interactions make complementary, collagen‐type‐specific contributions to adhesion

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