PKC and PI3K inhibition decreases FAK tyrosine phosphorylation and platelet spreading on high-density fibrinogen. Platelets were incubated with bisindolylmaleimide (10 μM; A-B), wortmannin (20 nM; A,C), or vehicle (control) and then allowed to adhere to wells precoated with fibrinogen. (A) Morphology of platelets adherent to low-density fibrinogen did not change with treatment with bisindolylmaleimide or wortmannin. Platelets adherent to high-density fibrinogen in the presence of these inhibitors showed less spreading than the control platelets. (B-C) Presence of PKC or PI3K inhibitors led to a decrease in FAK tyrosine phosphorylation in platelets adherent to high-density fibrinogen only. Noncontiguous lanes from a single blot are shown in both panels B and C. Results shown are representative of 3 independent experiments.