Human cell‐derived microparticles promote thrombus formation in vivo in a tissue factor‐dependent manner
Background: Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown. Objectives: To examine the in vivo thromboge...
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| Veröffentlicht in: | Journal of thrombosis and haemostasis Jg. 1; H. 12; S. 2561 - 2568 |
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| Hauptverfasser: | , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
Oxford, UK
Blackwell Science Inc
01.12.2003
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| Schlagworte: | |
| ISSN: | 1538-7933, 1538-7836, 1538-7836 |
| Online-Zugang: | Volltext |
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| Abstract | Background: Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown. Objectives: To examine the in vivo thrombogenicity of human microparticles. Methods: Microparticles were isolated from pericardial blood of cardiac surgery patients and venous blood of healthy individuals. Their numbers, cellular source, and tissue factor (TF) exposure were determined using flow cytometry. Their in vitro procoagulant properties were studied in a fibrin generation test, and their in vivo thrombogenicity in a rat model. Results: The total number of microparticles did not differ between pericardial samples and samples from healthy individuals (P = 0.786). In both groups, microparticles from platelets, erythrocytes, and granulocytes exposed TF. Microparticle‐exposed TF antigen levels were higher in pericardial compared with healthy individual samples (P = 0.036). Pericardial microparticles were strongly procoagulant in vitro and highly thrombogenic in a venous stasis thrombosis model in rats, whereas microparticles from healthy individuals were not [thrombus weights 24.8 (12.2–41.3) mg vs. 0 (0–24.3) mg median and range; P < 0.001]. Preincubation of pericardial microparticles with an inhibitory antibody against human TF abolished their thrombogenicity [0 (0–4.4) mg; P < 0.01], while a control antibody had no effect [19.6 (12.6–53.7) mg; P > 0.05]. The thrombogenicity of the microparticles correlated strongly with their TF exposure (r = 0.9524, P = 0.001). Conclusions: Human cell‐derived microparticles promote thrombus formation in vivo in a TF‐dependent manner. They might be the direct cause of an increased thromboembolic tendency in various patient groups. |
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| AbstractList | Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown.BACKGROUNDCirculating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown.To examine the in vivo thrombogenicity of human microparticles.OBJECTIVESTo examine the in vivo thrombogenicity of human microparticles.Microparticles were isolated from pericardial blood of cardiac surgery patients and venous blood of healthy individuals. Their numbers, cellular source, and tissue factor (TF) exposure were determined using flow cytometry. Their in vitro procoagulant properties were studied in a fibrin generation test, and their in vivo thrombogenicity in a rat model.METHODSMicroparticles were isolated from pericardial blood of cardiac surgery patients and venous blood of healthy individuals. Their numbers, cellular source, and tissue factor (TF) exposure were determined using flow cytometry. Their in vitro procoagulant properties were studied in a fibrin generation test, and their in vivo thrombogenicity in a rat model.The total number of microparticles did not differ between pericardial samples and samples from healthy individuals (P = 0.786). In both groups, microparticles from platelets, erythrocytes, and granulocytes exposed TF. Microparticle-exposed TF antigen levels were higher in pericardial compared with healthy individual samples (P = 0.036). Pericardial microparticles were strongly procoagulant in vitro and highly thrombogenic in a venous stasis thrombosis model in rats, whereas microparticles from healthy individuals were not [thrombus weights 24.8 (12.2-41.3) mg vs. 0 (0-24.3) mg median and range; P < 0.001]. Preincubation of pericardial microparticles with an inhibitory antibody against human TF abolished their thrombogenicity [0 (0-4.4) mg; P < 0.01], while a control antibody had no effect [19.6 (12.6-53.7) mg; P > 0.05]. The thrombogenicity of the microparticles correlated strongly with their TF exposure (r = 0.9524, P = 0.001).RESULTSThe total number of microparticles did not differ between pericardial samples and samples from healthy individuals (P = 0.786). In both groups, microparticles from platelets, erythrocytes, and granulocytes exposed TF. Microparticle-exposed TF antigen levels were higher in pericardial compared with healthy individual samples (P = 0.036). Pericardial microparticles were strongly procoagulant in vitro and highly thrombogenic in a venous stasis thrombosis model in rats, whereas microparticles from healthy individuals were not [thrombus weights 24.8 (12.2-41.3) mg vs. 0 (0-24.3) mg median and range; P < 0.001]. Preincubation of pericardial microparticles with an inhibitory antibody against human TF abolished their thrombogenicity [0 (0-4.4) mg; P < 0.01], while a control antibody had no effect [19.6 (12.6-53.7) mg; P > 0.05]. The thrombogenicity of the microparticles correlated strongly with their TF exposure (r = 0.9524, P = 0.001).Human cell-derived microparticles promote thrombus formation in vivo in a TF-dependent manner. They might be the direct cause of an increased thromboembolic tendency in various patient groups.CONCLUSIONSHuman cell-derived microparticles promote thrombus formation in vivo in a TF-dependent manner. They might be the direct cause of an increased thromboembolic tendency in various patient groups. Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown. To examine the in vivo thrombogenicity of human microparticles. Microparticles were isolated from pericardial blood of cardiac surgery patients and venous blood of healthy individuals. Their numbers, cellular source, and tissue factor (TF) exposure were determined using flow cytometry. Their in vitro procoagulant properties were studied in a fibrin generation test, and their in vivo thrombogenicity in a rat model. The total number of microparticles did not differ between pericardial samples and samples from healthy individuals (P = 0.786). In both groups, microparticles from platelets, erythrocytes, and granulocytes exposed TF. Microparticle-exposed TF antigen levels were higher in pericardial compared with healthy individual samples (P = 0.036). Pericardial microparticles were strongly procoagulant in vitro and highly thrombogenic in a venous stasis thrombosis model in rats, whereas microparticles from healthy individuals were not [thrombus weights 24.8 (12.2-41.3) mg vs. 0 (0-24.3) mg median and range; P < 0.001]. Preincubation of pericardial microparticles with an inhibitory antibody against human TF abolished their thrombogenicity [0 (0-4.4) mg; P < 0.01], while a control antibody had no effect [19.6 (12.6-53.7) mg; P > 0.05]. The thrombogenicity of the microparticles correlated strongly with their TF exposure (r = 0.9524, P = 0.001). Human cell-derived microparticles promote thrombus formation in vivo in a TF-dependent manner. They might be the direct cause of an increased thromboembolic tendency in various patient groups. Background: Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease states. To what extent these microparticles contribute to coagulation in vivo is unknown. Objectives: To examine the in vivo thrombogenicity of human microparticles. Methods: Microparticles were isolated from pericardial blood of cardiac surgery patients and venous blood of healthy individuals. Their numbers, cellular source, and tissue factor (TF) exposure were determined using flow cytometry. Their in vitro procoagulant properties were studied in a fibrin generation test, and their in vivo thrombogenicity in a rat model. Results: The total number of microparticles did not differ between pericardial samples and samples from healthy individuals (P = 0.786). In both groups, microparticles from platelets, erythrocytes, and granulocytes exposed TF. Microparticle‐exposed TF antigen levels were higher in pericardial compared with healthy individual samples (P = 0.036). Pericardial microparticles were strongly procoagulant in vitro and highly thrombogenic in a venous stasis thrombosis model in rats, whereas microparticles from healthy individuals were not [thrombus weights 24.8 (12.2–41.3) mg vs. 0 (0–24.3) mg median and range; P < 0.001]. Preincubation of pericardial microparticles with an inhibitory antibody against human TF abolished their thrombogenicity [0 (0–4.4) mg; P < 0.01], while a control antibody had no effect [19.6 (12.6–53.7) mg; P > 0.05]. The thrombogenicity of the microparticles correlated strongly with their TF exposure (r = 0.9524, P = 0.001). Conclusions: Human cell‐derived microparticles promote thrombus formation in vivo in a TF‐dependent manner. They might be the direct cause of an increased thromboembolic tendency in various patient groups. |
| Author | Hack, C. E. Sturk‐Maquelin, K. N. Meuleman, D. G. Biró, É. Sturk, A. Smit, M. J. Nieuwland, R. Vogel, G. M. T. |
| Author_xml | – sequence: 1 givenname: É. surname: Biró fullname: Biró, É. – sequence: 2 givenname: K. N. surname: Sturk‐Maquelin fullname: Sturk‐Maquelin, K. N. – sequence: 3 givenname: G. M. T. surname: Vogel fullname: Vogel, G. M. T. – sequence: 4 givenname: D. G. surname: Meuleman fullname: Meuleman, D. G. – sequence: 5 givenname: M. J. surname: Smit fullname: Smit, M. J. – sequence: 6 givenname: C. E. surname: Hack fullname: Hack, C. E. – sequence: 7 givenname: A. surname: Sturk fullname: Sturk, A. – sequence: 8 givenname: R. surname: Nieuwland fullname: Nieuwland, R. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/14738565$$D View this record in MEDLINE/PubMed |
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| References | 2001; 281 1986; 78 2002; 13 2002; 99 1997; 89 1997; 134 2000; 95 2003; 17 1998; 81 1940; 92 1999; 104 2001; 85 1994; 84 1990; 87 1988; 0 1989; 54 1997; 55 1993; 72 1997; 54 1997; 96 2002; 100 2000; 96 1982; 21 2002; 88 1976; 455 1997; 78 2000; 84 1999; 99 2000; 120 1996; 133 1999; 96 2003; 1 2000; 101 1996; 88 1998; 79 Sevinsky (10.1046/j.1538-7836.2003.00456.x_bb0110) 1996; 133 Bonderman (10.1046/j.1538-7836.2003.00456.x_bb0030) 2002; 99 Mulder (10.1046/j.1538-7836.2003.00456.x_bb0115) 1996; 88 Gando (10.1046/j.1538-7836.2003.00456.x_bb0165) 1998; 79 Quick (10.1046/j.1538-7836.2003.00456.x_bb0080) 1940; 92 Philippou (10.1046/j.1538-7836.2003.00456.x_bb0195) 2000; 84 Zillmann (10.1046/j.1538-7836.2003.00456.x_bb0035) 2001; 281 Bach (10.1046/j.1538-7836.2003.00456.x_bb0120) 1997; 89 Mallat (10.1046/j.1538-7836.2003.00456.x_bb0025) 1999; 99 Lee (10.1046/j.1538-7836.2003.00456.x_bb0145) 1993; 72 Siddiqui (10.1046/j.1538-7836.2003.00456.x_bb0040) 2002; 13 Mallat (10.1046/j.1538-7836.2003.00456.x_bb0155) 2000; 101 Giesen (10.1046/j.1538-7836.2003.00456.x_bb0015) 1999; 96 Brunner (10.1046/j.1538-7836.2003.00456.x_bb0085) 1976; 455 Vogel (10.1046/j.1538-7836.2003.00456.x_bb0090) 1989; 54 Warkentin (10.1046/j.1538-7836.2003.00456.x_bb0135) 1994; 84 Muller (10.1046/j.1538-7836.2003.00456.x_bb0050) 2003; 17 Amengual (10.1046/j.1538-7836.2003.00456.x_bb0190) 1998; 79 Suefuji (10.1046/j.1538-7836.2003.00456.x_bb0175) 1997; 134 Nemerson (10.1046/j.1538-7836.2003.00456.x_bb0010) 1988; 0 Bach (10.1046/j.1538-7836.2003.00456.x_bb0105) 1990; 87 Joop (10.1046/j.1538-7836.2003.00456.x_bb0070) 2001; 85 Misumi (10.1046/j.1538-7836.2003.00456.x_bb0180) 1998; 81 George (10.1046/j.1538-7836.2003.00456.x_bb0160) 1986; 78 Berckmans (10.1046/j.1538-7836.2003.00456.x_bb0055) 2001; 85 Rauch (10.1046/j.1538-7836.2003.00456.x_bb0095) 2000; 96 Shimura (10.1046/j.1538-7836.2003.00456.x_bb0170) 1997; 55 Nieuwland (10.1046/j.1538-7836.2003.00456.x_bb0060) 1997; 96 Balasubramanian (10.1046/j.1538-7836.2003.00456.x_bb0020) 2002; 100 Katopodis (10.1046/j.1538-7836.2003.00456.x_bb0150) 1997; 54 Scholz (10.1046/j.1538-7836.2003.00456.x_bb0045) 2002; 88 Nieuwland (10.1046/j.1538-7836.2003.00456.x_bb0065) 2000; 95 Combes (10.1046/j.1538-7836.2003.00456.x_bb0140) 1999; 104 Soejima (10.1046/j.1538-7836.2003.00456.x_bb0185) 1999; 99 Maquelin (10.1046/j.1538-7836.2003.00456.x_bb0075) 2000; 120 Sturk-Maquelin (10.1046/j.1538-7836.2003.00456.x_bb0100) 2003; 1 Dem Borne (10.1046/j.1538-7836.2003.00456.x_bb0130) 1997; 78 Lindhout (10.1046/j.1538-7836.2003.00456.x_bb0125) 1982; 21 |
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| Snippet | Background: Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various... Circulating microparticles of various cell types are present in healthy individuals and, in varying numbers and antigenic composition, in various disease... |
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| SubjectTerms | Adult Animals Blood Coagulation Blood Platelets Case-Control Studies Erythrocytes experimental animal model Female Flow Cytometry Granulocytes Humans Male microparticles Middle Aged Particle Size Pericardium Rats Thromboplastin - physiology Thrombosis - blood Thrombosis - etiology thrombus tissue factor |
| Title | Human cell‐derived microparticles promote thrombus formation in vivo in a tissue factor‐dependent manner |
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