Abstract
Platelet-activating factor (PAF) is a potent lipid autacoid identified as 1-0-alkyl-2-acetyl-sn-glycero-3-phosphocholine (figure 1). Originally isolated from immunoglobulin E-stimulated basophils as a potent inducer of platelet aggregation1, it soon became apparent that in addition to activation of platelets, PAF exerts diverse biological actions including stimulation of neutrophils, monocytes, and macrophages, increased vascular permeability, marked hemodynamic effects, and others2. It is now clear that PAF synthesis can be stimulated by various stimuli3 in many different cell types, some of which also release PAF into extracellular milieu. PAF actions are achieved at concentrations as low as 10−12 M in some systems and almost always by 10−9 M, suggesting a role as an intercellular messenger4. These observations have suggested that PAF plays a role both in normal physiological events and a variety of pathological responses. This chapter will emphasize the effects of PAF relevant to inflammatory responses and tissue injury. Some essential biochemical background of PAF will also be outlined.
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© 1991 Plenum Press, New York
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Yue, TL., Rabinovici, R., Feuerstein, G. (1991). Platelet-Activating Factor (PAF) - A Putative Mediator in Inflammatory Tissue Injury. In: Wong, P.YK., Serhan, C.N. (eds) Cell-Cell Interactions in the Release of Inflammatory Mediators. Advances in Experimental Medicine and Biology, vol 314. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6024-7_14
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DOI: https://doi.org/10.1007/978-1-4684-6024-7_14
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