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Fibrin Degradative Pathways and Angiogenesis in Healing, Atherosclerosis and Tumour Invasion

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Angiogenesis

Part of the book series: NATO ASI Series ((NSSA,volume 298))

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Abstract

Fibrin fragment E has been shown by us to be the component of fibrin degradation products (FDP) active in stimulating angiogenesis (1, 2). It is abundant in the healing wound (3), proliferative atherosclerotic plaques (4) and breast cancer (5). It is both a thrombin and plasmin dependant product, and stimulates cell proliferation in culture in serum rich medium in contrast with thrombin itself which requires serum free medium (6). We have attempted to study and locate the active site on this 35–40 kD molecule by various blocking antibody approaches. Fibrinogen is a highly conserved molecule, and this results in species similarity problems that confound conventional approaches. The mouse will not respond with antibodies to human fragment E, although it will to fragment D, the other major constituent of FDP. The rabbit and the rat will produce polyclonal antibodies against E that block the angiogenic effect of FDP.

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© 1998 Springer Science+Business Media New York

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Thompson, W.D., Stirk, C.M., Keating, A.J., Reid, A., Smith, E.B., Melvin, W.T. (1998). Fibrin Degradative Pathways and Angiogenesis in Healing, Atherosclerosis and Tumour Invasion. In: Maragoudakis, M.E. (eds) Angiogenesis. NATO ASI Series, vol 298. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9185-3_25

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  • DOI: https://doi.org/10.1007/978-1-4757-9185-3_25

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-9187-7

  • Online ISBN: 978-1-4757-9185-3

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