Abstract
Cardiovascular disease is the leading cause of death worldwide and arterial thrombosis, usually superimposed on atherosclerosis, is the immediate cause of acute myocardial infarction (AMI) and stroke.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Rissanen, A.M. and E.A. Nikkila, Coronary artery disease and its risk factors in families of young men with angina pectoris and in controls. Br. Heart J., 1977. 39(8): 875–83.
Williams, M.S. and P.F. Bray, Genetics of arterial prothrombotic risk states. Exp Biol Med (Maywood), 2001. 226(5): 409–19.
Boekholdt, S.M., et al., Genetic variation in coagulation and fibrinolytic proteins and their relation with acute myocardial infarction: a systematic review. Circulation, 2001. 104(25): 3063–8.
Yamada, Y., et al., Prediction of the risk of myocardial infarction from polymorphisms in candidate genes. N Engl J Med, 2002. 347(24): 1916–23.
Longstreth, W.T., Jr., et al., Risk of stroke in young women and two prothrombotic mutations: factor V Leiden and prothrombin gene variant (G20210A). Stroke, 1998. 29(3): 577–80.
Libby, P., Inflammation in atherosclerosis. Nature, 2002. 420(6917): p. 868–74.
Almus-Jacobs, F., Z.M. Ruggeri, and B. Savage, Specific synergy of multiple substrate-receptor interactions in platelet thrombus formation under flow. Cell, 1998. 94(5): 657–66.
Roy, S.N., G. Mukhopadhyay, and C.M. Redman, Regulation of fibrinogen assembly. Transfection of Hep G2 cells with B beta cDNA specifically enhances synthesis of the three component chains of fibrinogen. J Biol Chem, 1990. 265(11): 6389–93.
Margaglione, M., et al., Fibrinogen plasma levels in an apparently healthy general population--relation to environmental and genetic determinants. Thromb Haemost, 1998. 80(5): 805–10.
Scarabin, P.Y., et al., Associations of fibrinogen, factor VII and PAI-1 with baseline findings among 10,500 male participants in a prospective study of myocardial infarction--the PRIME Study. Prospective Epidemiological Study of Myocardial Infarction. Thromb Haemost, 1998. 80(5): 749–56.
Thompson, S.G., et al., Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. N Engl J Med, 1995. 332(10): 635–41.
Rezaee, F., et al., Increased hepatic fibrinogen Bbeta-gene transcription is not enough to increase plasma fibrinogen levels. A transgenic mouse study. Thromb Haemost, 2001. 85(6): 1025–30.
Ni, H., et al., Persistence of platelet thrombus formation in arterioles of mice lacking both von Willebrand factor and fibrinogen. J Clin Invest, 2000. 106(3): 385–92.
Tschopp, T.B., H.J. Weiss, and H.R. Baumgartner, Decreased adhesion of platelets to subendothelium in von Willebrand’s disease. J Lab Clin Med, 1974. 83(2): 296–300.
Keightley, A.M., et al., Variation at the von Willebrand factor (vWF) gene locus is associated with plasma vWF:Ag levels: identification of three novel single nucleotide polymorphisms in the vWF gene promoter. Blood, 1999. 93(12): 4277–83.
Sramek, A., et al., Decreased coagulability has no clinically relevant effect on atherogenesis: observations in individuals with a hereditary bleeding tendency. Circulation, 2001. 104(7): 762–7.
Ruggeri, Z.M., Mechanisms initiating platelet thrombus formation. Thromb Haemost, 1997. 78(1): 611–6.
Bray, P.F., Inherited diseases of platelet glycoproteins: considerations for rapid molecular characterization. Thromb Haemost, 1994. 72(4): 492–502.
Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty. The EPIC Investigation. N Engl J Med, 1994. 330(14): 956–61.
Platelet glycoprotein IIb/IIIa receptor blockade and low-dose heparin during percutaneous coronary revascularization. The EPILOG Investigators. N Engl J Med, 1997. 336(24): 1689–96.
Amoroso, G., et al., Pathophysiology of vascular endothelium and circulating platelets: implications for coronary revascularisation and treatment. Int J Cardiol, 2001. 79(2–3): 2–3.
Newman, P.J., Platelet alloantigens: cardiovascular as well as immunological risk factors? Lancet, 1997. 349(9049): 370–1.
Smyth, S.S., et al., Variable protection of beta 3-integrin--deficient mice from thrombosis initiated by different mechanisms. Blood, 2001. 98(4): 1055–62.
Toschi, V., et al., Tissue factor modulates the thrombogenicity of human atherosclerotic plaques. Circulation, 1997. 95(3): 594–9.
Badimon, J.J., et al., Local inhibition of tissue factor reduces the thrombogenicity of disrupted human atherosclerotic plaques: effects of tissue factor pathway inhibitor on plaque thrombogenicity under flow conditions. Circulation 1999. 99(14): 1780–7.
Bajaj, M.S., et al., Structure and biology of tissue factor pathway inhibitor. Thromb Haemost, 2001. 86(4): 959–72.
Abumiya, T., et al., Decreased plasma tissue factor pathway inhibitor activity in ischemic stroke patients. Thromb Haemost, 1995. 74(4): 1050–4.
Saigo, M., et al., Imbalance of plasminogen activator inhibitor-I/ tissue plasminogen activator and tissue factor/tissue factor pathway inhibitor in young Japanese men with myocardial infarction. Thromb Haemost, 2001. 86(5): 1197–203.
Kato, H., Regulation of functions of vascular wall cells by tissue factor pathway inhibitor: basic and clinical aspects. Arterioscler Thromb Vasc Biol, 2002. 22(4):. 539–48.
Nishida, T., et al., Adenovirus-mediated local expression of human tissue factor pathway inhibitor eliminates shear stress-induced recurrent thrombosis in the injured carotid artery of the rabbit. Circ Res 1999. 84(12): 1446–52.
Huang, Z.F., et al., Tissue factor pathway inhibitor gene disruption produces intrauterine lethality in mice. Blood, 1997. 90(3): 944–51.
Kunz, G., et al., Identification and characterization of a thrombomodulin gene mutation coding for an elongated protein with reduced expression in a kindred with myocardial infarction. Blood, 2000. 95(2): 569–76.
Dorffler-Melly, J., et al., Functional Thrombomodulin deficiency causes enhanced thrombus growth in a murine model of carotid artery thrombosis, in Experimental, clinical and meta-analytical studies of antithrombotic therapies in venous and arterial thrombosis, 2001: 149–58, University of Amsterdam: Amsterdam.
Weiler, H., et al., Characterization of a mouse model for thrombomodulin deficiency. Arterioscler Thromb Vasc Biol, 2001. 21(9): 1531–7.
Strater, R., et al., Prospective assessment of risk factors for recurrent stroke during childhood--a 5-year follow-up study. Lancet 2002. 360(9345): 1540–5.
Memarzadeh, S., et al., Urokinase plasminogen activator receptor: Prognostic biomarker for endometrial cancer. Proc Natl Acad Sci U S A, 2002. 99(16): 10647–52.
Fujii, S. and B.E. Sobel, Induction of plasminogen activator inhibitor by products released from platelets. Circulation 1990. 82(4): 1485–93.
Hamsten, A., et al., Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction. Lancet 1987. 2(8549): 3–9.
Senno, S.L. and L. Pechet, Clinical implications of elevated PAI-1 revisited: multiple arterial thrombosis in a patient with essential thrombocythemia and elevated plasminogen activator inhibitor-1 (PAI-1) levels: a case report and review of the literature. J Thromb Thrombolysis, 1999. 8(2): 105–12.
Farrehi, P.M., et al., Regulation of arterial thrombolysis by plasminogen activator inhibitor-1 in mice. Circulation, 1998. 97(10): 1002–8.
Fay, W.P., et al., Platelets inhibit fibrinolysis in vitro by both plasminogen activator inhibitor-I-dependent and -independent mechanisms. Blood, 1994. 83(2): 351–6.
Zhu, Y., P. Carmeliet, and W.P. Fay, Plasminogen activator inhibitor-1 is a major determinant of arterial thrombolysis resistance. Circulation, 1999. 99(23): 3050–5.
Asch, E. and E. Podack, Vitronectin binds to activated human platelets and plays a role in Platele aggregation. J Clin Invest, 1990. 85(5): 1372–8.
Mohri, H. and T. Ohkubo, How vitronectin binds to activated glycoprotein IIb-IIIa complex and its function in platelet aggregation. Am J Clin Pathol, 1991. 96(5): 605–9.
Konstantinides, S., et al., Plasminogen activator inhibitor-1 and its cofactor vitronectin stabilize arterial thrombi after vascular injury in mice. Circulation, 2001. 103(4): 576–83.
Eitzman, D.T., et al., Plasminogen activator inhibitor-1 and vitronectin promote vascular thrombosis in mice. Blood, 2000. 95(2): 577–80.
Konstantinides, S., K. Schafer, and D.J. Loskutoff, Do PAI-1 and vitronectin promote or inhibit neointima formation? The exact role of the fibrinolytic system in vascular remodeling remains uncertain. Arterioscler Thromb Vasc Biol, 2002. 22(12): 1943–5.
Peng, L., et al., Endogenous vitronectin and plasminogen activator inhibitor-1 promote neointima formation in murine carotid arteries. Arterioscler Thromb Vasc Biol, 2002. 22(6): 934–9.
de Waard, V., et al., Plasminogen activator inhibitor 1 and vitronectin protect against stenosis in a murine carotid artery ligation model. Arterioscler Thromb Vasc Biol, 2002. 22(12): p. 1978–83.
Kenchaiah, S., et al., Obesity and the risk of heart failure. N Engl J Med, 2002. 347(5): 305–13.
Laakso, M., Hyperglycemia and cardiovascular disease in type 2 diabetes. Diabetes, 1999. 48(5): 937–42.
Fuster, V., et al., The pathogenesis of coronary artery disease and the acute coronary syndromes (2). N Engl J Med, 1992. 326(5): 310–8.
Zhang, Y., et al., Positional cloning of the mouse obese gene and its human homologue. Nature, 1994. 372(6505): 425–32.
Nakata, M., et al., Leptin promotes aggregation of human platelets via the long form of its receptor. Diabetes, 1999. 48(2): 426–9.
Maruyama, I., M. Nakata, and K. Yamaji, Effect of leptin in platelet and endothelial cells. Obesity and arterial thrombosis. Ann N Y Acad Sci, 2000. 902: 315–9.
Strater, R, et al. Prospective assessment of risk factors for recurrent stroke during childhood. Lancet 2002 360: 1540–5.
Celi A, Merrill-Skoloff G, Gross P, et al. Thrombus formation: direct real-time observation and digital analysis of thrombus assembly in a living mouse by confocal and widefield intravital microscopy. J Thromb Hemost 2003, 1: 60–8
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2004 Springer Science+Business Media New York
About this chapter
Cite this chapter
Hansen, H., ten Cate, H. (2004). Mouse Models for Arterial Thrombosis: Does Clotting Make a Difference in Human Cardiovascular Disease?. In: Ince, C. (eds) The Physiological Genomics of the Critically Ill Mouse. Basic Science for the Cardiologist, vol 16. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0483-2_18
Download citation
DOI: https://doi.org/10.1007/978-1-4615-0483-2_18
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5099-6
Online ISBN: 978-1-4615-0483-2
eBook Packages: Springer Book Archive