How does fluoroaluminate activate human platelets?

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Abstract
Platelet activation induced by NaF or fluoroaluminate (AlF4-) was studied. The latter has been described to substitute for the .gamma.-phosphate group of the GTP molecule. With 10 mM-NaF, a concentration unable to induce any measureable Ca2+ mobilization (as measured with Indo 1), addition of AlCl3 potentiated platelet aggregation, thromboxane synthesis, diacylglycerol formation and p43 phosphorylation, without any increase in intracellular Ca2+. Neither phosphoinositide hydrolysis nor phosphatidic acid formation could be detected AlF4- induced the release through a granule centralization within a microtubule bundle, although no myosin light-chain phopshorylation could be detected. Addition of flurbiprofen (10 .mu.M) resulted in only partial inhibition of diacylglycerol formation, with no effect on the release reaction or on p43 phosphorylation. The present results suggest that AlF4--induced diacylglycerol formation is discussed. Moreover, these results bring evidence that there is no correlation between granule centralization and myosin light-chain phosphorylation.