Figure 5.

PP1cα^−/− platelets showed increased integrin outside–in signaling functions and the p38 inhibitor blocked these functions. (A) Increased adhesion of PP1cα^−/− platelets to fibrinogen at 60 min was blocked by water-soluble p38 inhibitor SB203580. n = 4. (B) Enhanced fibrin clot retraction from platelet-rich plasma of PP1cα^−/− mice was attenuated with a p38 inhibitor. n = 6–8. (C) Whole blood from PP1cα^−/− mice perfused over immobilized collagen at 1000^s−1 resulted in an increased in vitro thrombus coverage that was blocked by a p38 inhibitor. Images acquired after 4 min of perfusion were quantified as integrated fluorescence intensity from three independent experiments. * p < 0.05. The differences between p38 inhibitor-treated platelets and untreated platelets were not statistically significant (p > 0.05; ns).