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PAF, a potent proinflammatory mediator, looking for its role in the pathogenesis of joint damage
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Introduction |
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Cell activation is accompanied by remodelling of its membrane components producing structurally diverse intracellular and extracellular lipids that seem to be essential in signal transduction, cell-cell communication, and as mediators in inflammation and pathophysiological mechanisms.1 Phospholipases are pivotal enzymes in the generation of these lipids, including eicosanoids (mostly prostaglandins), platelet activating factor (PAF), diacylglycerides, and other newly discovered bioactive autacoids.
PAF is a potent proinflammatory phospholipid mediator, involved in the pathogenesis of lung, liver, cardiovascular, renal, and other diseases.2 The gene coding for the human specific PAF receptor has recently been cloned from leucocytes showing homology to G protein coupled receptors.3
During the inflammatory arthritic process there are basically tissue
damage phenomena combined with reparative processes. In brief,
endothelial damage is followed by inflammatory cell infiltration in the
perivascular area and synovial membrane. Furthermore, hyperplasia of
synovial cells and accumulation of fibronectin and other matrix
proteins are also seen. These
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