The presence and stereospecific position of the 2-acetyl group are critical for the interaction of PAF-acether with platelets to induce aggregation and desensitization.
Hypothesis-generating for PAF-acether mechanisms; leaves open translation to human platelet disorders or thrombosis.
PAF-acether is a 1-O-alkyl-2 acetyl-sn-glycerol-3-phosphorylcholine which triggers platelet aggregation independently from ADP release and thromboxane A2 formation. PAF-acether-aggregated rabbit platelets did not respond to a second challenge with the same agonist, but still aggregated to arachidonic acid. This desensitization to PAF-acether was a dose-dependent phenomenon. Specific cross-desensitization to PAF-acether was achieved using PAF-acether from four cellular origins, synthetic PAF-acether and its 2-propionyl analogue. Conversely, 2-lyso-PAF-acether and PAF-acether enantiomer were unable to induce specific desensitization. These results suggest that PAF-acether, whatever its origin, exhibits identical active molecular site, and that the presence and the stereospecific position of the 2-acetyl group are critical for the interaction of PAF-acether with platelets.
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Keraly et al. (1982) studied this question.
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