Ck2β deficiency results in significantly reduced platelet adhesion and thrombus stability under high arterial shear rates as well as abrogated thrombotic vascular occlusion in vivo, whereas primary hemostasis is not significantly affected. (A) Flow chamber analysis of platelet adhesion to collagen and thrombus formation in vitro under high arterial shear rates. Whole blood from ck2β^fl/fl and ck2β^−/− mice was perfused over a collagen-coated surface for 5 minutes at a shear rate of 1700 s⁻¹. Arithmetic means ± standard errors of the means (n = 6; right) and representative phase contrast images (left) of surface coverage are shown. Bar represents 50 µm. (B) Time to arterial occlusion after FeCl₃-induced injury of mesenteric arterioles (right, n = 12) and representative images of occlusive in vivo thrombus formation after 0, 10, and 20 minutes (left) in ck2β^fl/fl and ck2β^−/− mice. Each dot represents 1 individual mouse. Bar represents 50 µm. (C) Representative images of in vivo thrombus formation after 0, 2.5, 5, 10, and 20 minutes (left) and time to arterial occlusion after FeCl₃-induced injury of carotid arteries (upper right, n = 12) and representative immunohistological H&E staining (lower right) of occlusive in vivo thrombus formation after 7 minutes in ck2β^fl/fl and ck2β^−/− mice. Each dot represents 1 individual mouse. Bar represents 100 µm. (D) Arithmetic means ± standard errors of the means (n = 6) of integrated fluorescence intensity of adherent platelets after perfusion of whole blood from ck2β^fl/fl (blue dots) and ck2β^−/− (gray dots) mice over a collagen-coated surface representing thrombus growth in vitro over 5 minutes. (E) Tail bleeding time measured after amputating the tail tip of ck2β^fl/fl and ck2β^−/− mice. Each dot represents 1 individual mouse (n = 36). Unpaired Student t test in panels A-E. **P < .01.