Platelet adhesion to fibronectin in flow: dependence on surface concentration and shear rate, role of platelet membrane glycoproteins GP IIb/IIIa and VLA-5, and inhibition by heparin

Beumer, S.; IJsseldijk, Martin J. W.; Groot, Philip G. de; Sixma, Jan J.

doi:10.1182/blood.v84.11.3724.bloodjournal84113724

Cited by 88 publications

(45 citation statements)

References 44 publications

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“…Another characteristic of fibronectin and fibrinogen is that both these proteins are capable of capturing platelets under flow conditions [28,29]. In our hands, fibrinogen was the strongest platelet adhesive surface under both arterial and venous shear rates.…”

Section: Discussionsupporting

confidence: 54%

A fibronectin‐fibrinogen‐tropoelastin coating reduces smooth muscle cell growth but improves endothelial cell function

Tersteeg

Roest

Mak-Nienhuis

et al. 2012

J Cellular Molecular Medi

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Reendothelialization of the stent surface after percutaneous coronary intervention (PCI) is known to be an important determinant of clinical outcome. We compared the effects of biological stent coatings, fibronectin, fibrinogen and tropoelastin, on human umbilical vein endothelial cell (HUVEC) and vascular smooth muscle cell (VSMC) characteristics. Umbilical cord arterial segments were cultured on coated surfaces and VSMC outgrowth (indicating proliferation and migration) was measured after 12 days. mRNA was isolated from HUVEC and VSMC cultured on these coatings and gene expression was profiled by QPCR. Procoagulant properties of HUVEC were determined by an indirect chromogenic assay which detects tissue factor activity. The varying stent coatings influence VSMC outgrowth: 31.2 ± 4.0 mm2 on fibronectin, 1.6 ± 0.3 mm2 on tropoelastin and 8.1 ± 1.5 mm2 on a mixture of fibronectin/fibrinogen/tropoelastin, although HUVEC migration remains unaffected. Culturing HUVEC on tropoelastin induces increased expression of VCAM-1 (13.1 ± 4.4 pg/ml), ICAM-1 (5.1 ± 1.3 pg/ml) and IL-8 (11.6 ± 3.1 pg/ml) compared to fibronectin (0.7 ± 0.2, 0.8 ± 0.2, 2.3 ± 0.5 pg/ml, respectively), although expression levels on fibronectin/fibrinogen/tropoelastin remain unaltered. No significant differences in VCAM-1, ICAM-1 and IL-8 mRNA expression are found in VSMC. Finally, HUVEC cultured on tropoelastin display a fivefold increased tissue factor activity (511.6 ± 26.7%), compared to cells cultured on fibronectin (100 ± 3.9%) or fibronectin/fibrinogen/tropoelastin (76.3 ± 25.0%). These results indicate that tropoelastin inhibits VSMC migration but leads to increased inflammatory and procoagulant markers on endothelial cells. Fibronectin/fibrinogen/tropoelastin inhibits VSMCs while compensating the inflammatory and procoagulant effects. These data suggest that coating a mixture of fibronectin/fibrinogen/tropoelastin on a stent may promote reendothelialization, while keeping unfavourable processes such as restenosis and procoagulant activity limited.

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Section: Discussionsupporting

confidence: 54%

A fibronectin‐fibrinogen‐tropoelastin coating reduces smooth muscle cell growth but improves endothelial cell function

Tersteeg

Roest

Mak-Nienhuis

et al. 2012

J Cellular Molecular Medi

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“…Antibodies against the VWF GPIb binding site inhibited platelet adhesion to TSP-1 at 1600 s -1 and 1700 s -1 to ~30%. Unlike platelet adhesion to fibronectin (27), platelet mediated adhesion to TSP-1 does not depend on VWF.…”

Section: Discussionmentioning

confidence: 87%

“…They suggested that fibronectin from the α-granules might be the ligand. However, platelet adhesion to fibronectin has an optimum at 300 s -1 (27) and, at arteriole shear rates, platelets do not adhere to fibronectin. TSP-1 is a much better candidate to promote thrombus formation in coronary or cerebral arteries.…”

Section: Discussionmentioning

confidence: 99%

Thrombospondin‐1 mediates platelet adhesion at high shear via glycoprotein Ib (GPIb): an alternative/backup mechanism to von Willebrand factor

et al. 2003

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Acute thrombotic arterial occlusion is the leading cause of morbidity and mortality in the Western world. Von Willebrand factor is thought to be the only indispensable adhesive substrate to promote thrombus formation in high shear environments. We found that thrombospondin-1, a glycoprotein enriched in arteriosclerotic plaques, might function as an alternative substrate for thrombus formation. Platelets adhered to thrombospondin-1 in a shear dependent manner with an optimum shear as found in stenosed arteries. Adhesion is extremely firm, with no detachment of platelets up to a shear rate of 4000 s(-1). Experiments using platelets from a patient completely lacking von Willebrand factor showed that von Willebrand factor is not involved in platelet binding to thrombospondin-1. Platelet adhesion to thrombospondin-1 is not mediated via beta3-integrins or GPIa. CD36 partially mediates the adhesion of pre-activated platelets. We identified GPIb as high shear adhesion-receptor for thrombospondin-1. Soluble GPIb, as well as antibodies against the GPIb, blocked platelet adhesion almost completely. The new discovered thrombospondin-1-GPIb adhesion axis under arterial shear conditions might be important, not only during thrombus formation but also for pathological processes where other cells bind to the endothelium or subendothelium, including arteriosclerosis, inflammation and tumor metastasis, and a promising therapeutic target.

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“…Standard platelet aggregometry ( Kirlough‐Ratbone et al , 1983 ) is limited to platelet counts above 100.0 × 10 9 /l and its application to risk assessment among thrombocytopenic patients is therefore limited. Standard bleeding time is poorly standardized and has major practical limitations ( Rodgers & Levin, 1991), and other recently described methods of testing platelet function have not yet proved their clinical applicability ( Michelson, 1996; Ikeda et al , 1991 ; Beumer et al , 1994 ; Baumgartner, 1974; Diaz‐Ricart et al , 1994 ; Kundu et al , 1995 ; Mammen et al , 1990 ).…”

mentioning

confidence: 99%

Cone and platelet analyser (CPA): a new test for the prediction of bleeding among thrombocytopenic patients

Kenet

Lubetsky²,

Шенкман³

et al. 1998

Br J Haematol

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The risk of bleeding among thrombocytopenic patients was evaluated using our new cone and platelet analyser (CPA) test. Using this test, adherence of platelets was quantitated on extracellular matrix and expressed as percent of surface coverage (SC) and the average size (AS) of aggregates. 42 thrombocytopenic patients with ITP (n=23), post chemotherapy (n= 12) and others (n= 7) were tested over a total of 82 visits. On each visit, complete blood count and CPA tests were performed and patients were evaluated for evidence of bleeding (found in 40 visits). Bleeding patients had significantly lower platelet counts (27.4 +/- 22.0 v 47.1 +/- 21.0 x 10(9)/l), lower haematocrit values (30.2 +/- 8.1 v 35.2 +/- 6.6%), lower MPV (6.83 +/-1.89 v 8.98 +/- 1.13 fl), and lower SC (4.87 +/- 3.95 v 10.33 +/-5.48%) and AS (33.99 +/- 14.94 v 52.9 +/- 24.34 microm2). Univariate analysis yielded platelet count < or =20.0 x 10(9)/l, MPV < or =8 fl, haematocrit <35%, SC <5%, AS< or =40 microm2 as significantly associated with bleeding, whereas only MPV and SC were associated with bleeding (OR 6.95, CI 2.25-21.46 and OR 4.27, CI 1.29-14.16, respectively) by multivariate analysis. When taken together, 21/22 of patients (95%) with both low SC (<5%) and low MPV (<8.0 fl) had bleeding symptoms, whereas only 9/43 (21%) patients with both these parameters above these values experienced bleeding symptoms. We conclude that the CPA test and the parameter SC (<5%) together with MPV (< or =8 fl) might be used as independent predictors of bleeding in the management of thrombocytopenic patients.

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Platelet adhesion to fibronectin in flow: dependence on surface concentration and shear rate, role of platelet membrane glycoproteins GP IIb/IIIa and VLA-5, and inhibition by heparin

Cited by 88 publications

References 44 publications

A fibronectin‐fibrinogen‐tropoelastin coating reduces smooth muscle cell growth but improves endothelial cell function

A fibronectin‐fibrinogen‐tropoelastin coating reduces smooth muscle cell growth but improves endothelial cell function

Thrombospondin‐1 mediates platelet adhesion at high shear via glycoprotein Ib (GPIb): an alternative/backup mechanism to von Willebrand factor

Cone and platelet analyser (CPA): a new test for the prediction of bleeding among thrombocytopenic patients

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