Abstract
Platelet interactions with the blood vessel wall following injury influence both the acute thrombotic event (platelet/vessel wall adhesion) and the chronic pathogenesis of arteriosclerosis (chronic vessel wall thickening and occlusion). Platelets are thought not to interact with the healthy intact endothelium, but only to adhere to vessel wall components exposed following endothelial cell damage and vessel wall injury (1–3). When platelets adhere to the injured vessel wall, they release a number of constituents which facilitate further platelet activation (3), activation of the coagulation cascade (1), and/or are mitogenic, facilitating smooth muscle cell proliferation and hyperplasia (4). Endothelial cells also synthesize and release a number of constituents which counterbalance the platelet responses, thereby enhancing fibrinolysis, inhibiting coagulation and preventing platelet aggregation and adhesion (5–7). Recently, with the development of endothelial cell culture techniques and a number of molecular biologic tools, we have learned that platelets and other blood cells actively interact not only with the injured vessel wall, but also with the intact endothelium itself. In this chapter, we will focus on the latter interaction and specifically on endothelial cell fatty acid metabolism and its possible consequence on the reactivity of adhesion molecule receptors on the surface of the intact endothelium which in turn may influence platelet/vessel wall interactions.
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Buchanan, M.R., Bertomeu, M.C., Brister, S.J., Haas, T.A. (1991). Eicosanoid Metabolism and Endothelial Cell Adhesion Molecule Expression: Effects on Platelet/Vessel Wall Interactions. In: Gotlieb, A.I., Langille, B.L., Fedoroff, S. (eds) Atherosclerosis. Altschul Symposia Series, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3754-0_17
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DOI: https://doi.org/10.1007/978-1-4615-3754-0_17
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