J. Biol. Chem., Vol. 258, Issue 12, 7241-7244, Jun, 1983
Shape change induced in human platelets by platelet-activating factor. Correlation with the formation of phosphatidic acid and phosphorylation of a 40,000-dalton protein
EG Lapetina and FL Siegel
Washed human platelets that have been separated from plasma in the presence
of prostacyclin are activated by the addition of platelet activating factor
(PAF). Activation (shape change, serotonin release, and aggregation)
correlates closely with the formation of phosphatidic acid and the
phosphorylation of a 40,000-dalton protein. Platelet shape change,
formation of phosphatidic acid, and protein phosphorylation precede
aggregation and are induced at lower concentrations of PAF than those
required to induce release of serotonin and platelet aggregation. Platelet
shape change, formation of phosphatidic acid, and protein phosphorylation
induced by PAF are not affected by trifluoperazine or indomethacin. This
indicates that these responses are independent of the liberation of
arachidonic acid from platelet phospholipids and the metabolism of
arachidonic acid via cyclooxygenase and lipoxygenase. These responses are,
however, inhibited by prostacyclin. Platelet shape change is the first
measurable physiologic response to platelet agonists and may be associated
with the stimulation of phospholipase C, inducing formation of
1,2-diacylglycerol and its phosphorylated product, phosphatidic acid.
Transient formation of 1,2-diacylglycerol may also induce the specific
activation of the protein kinase C that phosphorylates a 40,000-dalton
protein.
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