PKCδ negatively regulates filopodia formation in mouse platelets. (A) Washed platelets from either wild-type (WT) or PKCδ^–/– (δ-KO) mice were preincubated for 15 minutes with either rottlerin (5 μM) or DMSO as control (vehicle) as indicated. Platelets were added to collagen-coated coverslips and allowed to settle on the surface and adhere to collagen fibers under static conditions. (i) Images shown are for platelets allowed to adhere to the collagen-coated surface for 40 minutes, representative of 5 independent experiments. The perimeter (ii) and number (iii) of adherent platelets were measured 0, 10, 20, 30, or 40 minutes after being dispensed onto the collagen-coated surface. In the absence of rottlerin, the differences in perimeter (at 10, 20, 30, and 40 minutes) between WT and PKCδ^–/– (δ-KO) platelets were statistically significant (P < .01), while no significant difference was detected (P > .05) for the number of adherent platelets. In the presence of rottlerin, the difference in perimeter between PKCδ^–/– (δ-KO) and WT platelets was not significant (P > .05). Data shown are mean ± SEM from 3 independent experiments. (B) Washed platelets from either wild-type (WT) or PKCδ^–/– (δ-KO) mice were preincubated for 15 minutes with either NSC23766 (200 μM) or DMSO as control (vehicle) as indicated. Platelets were added to collagen-coated coverslips and allowed to settle on the surface and adhere to collagen fibers under static conditions. (i) Images shown are for platelets allowed to adhere to the collagen-coated surface for 40 minutes, representative of 3 independent experiments. The perimeter (ii) and number (iii) of adherent platelets were measured 0 and 40 minutes after being dispensed onto the collagen-coated surface. The differences in perimeter between WT or PKCδ^–/– (δ-KO) platelets at 40 minutes were statistically significant in the presence or absence of NSC23766 (P < .01). Values shown are mean ± SEM from 3 independent experiments, and the statistical differences were analyzed by 1-way ANOVA.