Key result
Thrombin stimulation of intact platelets caused a 57-62% fall in the pertussis toxin substrate within 10-60 seconds, an effect modulated by protein kinase C and cyclic AMP-dependent protein kinase.
Why the study?
Does thrombin stimulation alter G-protein oligomer dissociation in intact platelets, and how is this modulated by PMA and prostaglandin D2?
Does thrombin stimulation alter G-protein oligomer dissociation in intact platelets, and how is this modulated by PMA and prostaglandin D2?
Activation of thrombin receptors promotes the dissociation of G-protein oligomers to release free alpha-subunits in platelets, an effect modulated by protein kinase C and cyclic AMP-dependent protein kinase.
Answers are grounded in this paper and cite their sources.
Rapid platelet G-protein modulation by stimulation; leaves open its relevance to thrombotic pathways pending in vivo validation.
Intact platelets were stimulated with thrombin and the amount of GTP-binding protein (G-protein) oligomers was assessed by measuring ADP ribosylation of 40-41 kDa protein by pertussis toxin in isolated membranes. The toxin substrate fell by 57-62% in 10-60 s, but then returned towards normal over 5 min. Recovery was greatly enhanced by removal of thrombin from receptors with hirudin. Phorbol myristate acetate increased ADP-ribosylatable protein, but only back to initial levels prior to PMA. In contrast prostaglandin D2 plus theophylline (which increase cyclic AMP) did not increase ADP ribosylation, but could completely block the fall of the toxin substrate caused by thrombin. These results indicate that activation of thrombin receptors promotes the dissociation of G-protein oligomers to release free alpha-subunits, and this effect can be modulated by protein kinase C and cyclic AMP-dependent protein kinase. The possible relationships of these findings to the regulation of stimulus-response coupling in platelets is discussed.
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Halenda et al. (1986) studied this question. Thrombin, phorbol myristate acetate, and prostaglandin D2 was evaluated on Amount of GTP-binding protein oligomers assessed by measuring ADP ribosylation of 40-41 kDa protein by pertussis toxin. Thrombin stimulation of intact platelets caused a 57-62% fall in the pertussis toxin substrate within 10-60 seconds, an effect modulated by protein kinase C and cyclic AMP-dependent protein kinase.
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