PKCδ negatively regulates actin polymerization in platelets. (A) F-actin quantification in human platelets adherent to collagen-coated or CRP-coated surfaces in the absence or presence of rottlerin (5 μM). (B) Wild-type (WT) or PKCδ–/– mouse platelets adherent to CRP-coated surfaces. Platelets were fixed 40 minutes after addition to the coated surfaces, permeabilized, and stained with TRITC-phalloidin. Fluorescence labeling was detected by confocal microscopy and quantified using Leica Confocal Software. Data represent mean ± SEM (n = 4), and the statistical significance of difference was analyzed by 1-way ANOVA (*P < .01, comparison between results in the absence or presence of rottlerin or between WT and PKCδ–/– mouse platelets). Images below the graphs show representative examples of platelets obtained under the same conditions indicated in the bar graph and stained with TRITC-phalloidin (top row), with corresponding phase-contrast images (bottom row).