Insulin-induced expression of prostacyclin receptors on platelets is mediated through ADP-ribosylation of Gi alpha protein.

The binding of insulin in physiological amounts to human blood platelets, which increases adenylate cyclase-linked prostacyclin receptor numbers on the cell surface, was found to be directly related to the ADP-ribosylation of the Gi alpha. Conversely, resuspension of the insulin-treated platelets in the hormone-free medium decreased both the prostaglandin receptor numbers and ADP-ribosylation of Gi alpha. Furthermore, incubation of platelets with pertussis toxin or its A-protomer, which ADP-ribosylates Gi alpha, also stimulated the binding of the prostanoid. These results suggest that the increase of prostacyclin receptor numbers in platelets is mediated through the ADP-ribosylation of Gi alpha.