Subendothelial proteins and platelet adhesion. von Willebrand factor and fibronectin, not thrombospondin, are involved in platelet adhesion to extracellular matrix of human vascular endothelial cells.

Houdijk, Wim P.M.; Groot, Philip G. de; Nievelstein, P F; Sakariassen, Kjell S.; Sixma, JJ

doi:10.1161/01.atv.6.1.24

Cited by 122 publications

(65 citation statements)

References 28 publications

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“…These findings are consistent with recent data showing that TSP in the pericellular matrix of endothelial cells is not required for normal platelet adhesion. 13 Anti-TSP, however, did neutralize the axial increase in thrombus dimensions as observed at a shear rate of 2600 s" 1 . This surprising observation indicates that platelets deposited upstream may influence passing platelets to interact more efficiently further downstream.…”

Section: Discussionmentioning

confidence: 82%

“…66 Indeed, decreased axial platelet deposition on endothelial cells. 13 However, both proteins play a role in platelet-platelet cohesion, as was demonstrated in ex vivo perfusion experiments with blood from patients with von Willebrand's disease 14 and in studies with the aggregometer using antibodies against TSP. 1516 We report on characterization and quantitation of plateletsurface interactions in flowing citrated blood at welldefined axial positions on a variety of surfaces.…”

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confidence: 98%

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Axial dependence of platelet-collagen interactions in flowing blood. Upstream thrombus growth impairs downstream platelet adhesion.

Sakariassen

Baumgartner

1989

Arteriosclerosis

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Vascular subendothelium and collagenous surfaces were exposed to flowing cltrated blood. Platelet interactions with these surfaces were Investigated at various axial distances from the upstream end of the exposed surfaces. A pronounced axial decrease In surface coverage with platelets and in thrombus dimensions was encountered on collagenous surfaces. This phenomenon was observed at shear rates of 200 to 2000 s~\ but was most pronounced at low shear rates (<650 s~1). After 5 minutes of perfusion at a shear rate of 650 s~\ 4.6x10* platelets were deposited on the most upstream 20 mm 2 of the collagen surface, In contrast to 2.2x10° platelets/ 20 mm 2 14 mm farther downstream. Depletion of von Wlllebrand factor and/or thrombospondin from the boundary layer of the blood flow was not responsible for this. Collagen-bound von Wlllebrand factor enhanced the surface coverage with platelets without affecting the axial decrement, while pretreatment of the collagen surface with thrombospondin had no effect at all. However, partial Inhibition of thrombus growth by aspirin reduced the axial decrements, and less thrombogenlc surfaces as human and rabbit subendothelium, which induced only a few small thrombi, produced virtually no axial differences In platelet adhesion. Raising the shear rate to 2600 s~1 also gave no axial differences In platelet-collagen adhesion; It did, however, give an axial Increase In thrombus dimensions. This Increase was neutralized after the addition of antibody against human platelet thrombospondin to the blood. Our data are consistent with the view that platelet-surface Interactions are limited by the arrival of platelets to the surface at shear rates below 650 s~1. Surfaces that Induce rapid-growing upstream thrombi may deplete the boundary layer for platelets, resulting In decreased platelet adhesion and thrombus growth farther downstream. At higher shear rates, when the platelet supply to the surface Is not a limiting factor, thrombospondin released from upstream thrombi appears to enhance downstream thrombus growth and/or thrombus stability. (Arteriosclerosis 9:33-42, January/February 1989)

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Section: Discussionmentioning

confidence: 82%

mentioning

confidence: 98%

Axial dependence of platelet-collagen interactions in flowing blood. Upstream thrombus growth impairs downstream platelet adhesion.

Sakariassen

Baumgartner

1989

Arteriosclerosis

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“…First, citrate-anticoagulated whole blood was perfused over deendothelialized human umbilical artery segments and over sprayed collagen (fibrillar type I). Both surfaces induce platelet adhesion as well as platelet aggregation; collagen as one of the constituents of the deeper vessel wall, however, is a more potent stimulus ofplatelet aggregation ( 17). In this way we determined that increased vWF levels and red blood cell rigidity and the in vitro hyperaggregability in nephrosis do not coincide with an increased platelet-vessel wall interaction under physiologic flow conditions.…”

Section: )mentioning

confidence: 97%

Thrombus formation and platelet-vessel wall interaction in the nephrotic syndrome under flow conditions

Zwaginga¹,

Koomans²,

Sixma³

et al. 1994

Pediatr Nephrol

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Increased in vitro platelet aggregability and hypercoagulability are generally held to be main determinants in the prethrombotic state in nephrosis. In vivo, however, thrombotic events depend on the dynamic interaction of flowing blood with the vessel wall. The present study confirms that aggregability of platelets of nephrotic patients is significantly increased by mere stirring or by exogenous stimuli as adenosine diphosphate and arachidonic acid. Moreover, the nephrotic patients have high von Willebrand factor and decreased red blood cell deformability, which normally increase platelet-vessel wall interaction. However, perfusion studies under well-defined flow conditions, in which anticoagulated nephrotic blood was exposed to deendothelialized human umbilical artery segments and sprayed collagen, showed normal platelet adhesion and only a modest increase in the deposition of platelet aggregates. This suggests that some factor counteracts platelet-vessel wall interaction under flow conditions in the nephrotic syndrome. When tissue factor associated with endothelial extracellular matrix (ECM) was allowed to generate thrombin, perfusions with nephrotic blood over this ECM resulted in a strong increase in fibrin generation. The capacity of patient blood to form increased amounts of fibrin appeared strongly correlated with the level of hyperfibrinogenemia. Platelet adhesion as well as aggregation in these experiments was even decreased below control values. This suggests that fibrin coverage may block the direct contact between blood platelets and matrix. We therefore also studied the isolated effect of high fibrinogen on platelet-vessel wall interaction by increasing fibrinogen concentrations in normal blood. Modulation of fibrinogen concentrations in normal blood could mimic all the observations in nephrotic blood: platelet aggregation in suspension increased with increasing concentrations of fibrinogen, while platelet adhesion and aggregate formation under flow conditions decreased. In perfusions over tissue factor-rich matrix, fibrin deposition increased. Therefore, our observations indicate that nephrotic hyperaggregability in suspension is not associated with increased platelet vessel wall-interaction under flow conditions. The latter is probably counteracted by high levels of fibrinogen. Our observations further suggest that hyperfibrinogenemia may be a major thrombotic risk factor in nephrosis by inducing more fibrin depositions. (J. Clin. Invest. 1994. 93:204-211.)

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“…In this study, we demonstrated that the quantity of a certain ECM component was different between ECMs of different origin. There was a higher amount of FN in SMC-ECM, which can be regarded as responsible for the platelet adhesion to the ECM, 27 in parallel with higher amount of LN, which has been proven not to cause platelet aggregation. 28 So, the available data about the component differences between EC-ECM and SMC-ECM were not sufficient to elucidate their differences in hemocompatibility.…”

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confidence: 98%

“…However, it is well known that von Willebrand factor (vWF) is specifically expressed and deposited onto the ECM by the ECs, but not by SMCs, and some researchers thought that the adhesion site in EC-ECM for platelets was probably a complex of vWF, FN, and collagen molecules. 27 So, the lack of vWF may be partly responsible for the fewer platelet adhesion on SMC-ECM than on EC-ECM.…”

mentioning

confidence: 99%

Effect of Tissue Specificity on the Performance of Extracellular Matrix in Improving Endothelialization of Cardiovascular Implants

Yang

Zhu

et al. 2013

Tissue Engineering Part A

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Natural extracellular matrix (ECM) deposited in situ by cultured endothelial cells (ECs) has been proven effective in accelerating endothelialization of titanium (Ti) cardiovascular implants (CVIs) in our previous studies. In this study, the ECM deposited by smooth muscle cells (SMCs) was used in comparison to investigate the effects of tissue specificity of the ECM on the ability to accelerate endothelialization of CVIs. The results demonstrated that the ECM deposited by ECs and SMCs (EC-ECM, SMC-ECM, respectively) differed considerably in components and fibril morphology. Surface modification of Ti CVIs with both types of natural ECM was effective in improving their in vitro hemocompatibility and cytocompatibility simultaneously. However, the endothelialization of ECM-modified Ti CVIs in a canine model demonstrated a high tissue specificity of the ECM. Although the ECM deposited by SMCs (SMC-ECM) induced fewer platelet adhesion and sustained better growth and viability of ECs in vitro, its performance in accelerating in vivo endothelialization of Ti CVIs was extremely poor. In contrast, the ECM deposited by ECs (EC-ECM) led to complete endothelium formation in vivo.

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Subendothelial proteins and platelet adhesion. von Willebrand factor and fibronectin, not thrombospondin, are involved in platelet adhesion to extracellular matrix of human vascular endothelial cells.

Cited by 122 publications

References 28 publications

Axial dependence of platelet-collagen interactions in flowing blood. Upstream thrombus growth impairs downstream platelet adhesion.

Axial dependence of platelet-collagen interactions in flowing blood. Upstream thrombus growth impairs downstream platelet adhesion.

Thrombus formation and platelet-vessel wall interaction in the nephrotic syndrome under flow conditions

Effect of Tissue Specificity on the Performance of Extracellular Matrix in Improving Endothelialization of Cardiovascular Implants

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