Myeloid specific α9^−/− mice are less susceptible to experimental arterial thrombosis. (A) Western blot analysis of α9 integrin from bone marrow-derived neutrophils (top). Quantification (n = 3 mice/group) (bottom). (B) Representative microphotographs of carotid artery thrombus (7.5% FeCl₃ injury) (left). Platelets were labeled ex vivo with calcein green. Time to occlusion (n = 11-12 mice/group) (middle). Rate of thrombus growth (n = 11-12 mice/group) (right). The rate of thrombus growth over a period of 2 minutes was calculated by dividing the area of the thrombus at time (n) by the area of the same thrombus at time (0) (defined as the time point at which the thrombus diameter first reached 30 μm). Slopes over time showed that the rate of thrombus growth in the α9^fl/flLysMCre⁺ mice (slope, 0.1758) was decreased when compared with α9^fl/fl mice (slope, 0.3575). *P < .05. (C) Tail bleeding assay (n = 8-10 mice/group). (D) MPO quantification by ELISA in carotid artery thrombus (n = 6-8 mice/group). (E) Representative immunofluorescence images of sections stained with anti-neutrophil elastase antibody. Scale bar, 100 μm. Boxed region is magnified to show colocalization of Hoechst/neutrophil elastase-positive cells (left). Quantification of neutrophil elastase-positive cells (n = 5-7 mice/group) (right). Value for each mouse represents a mean from 3 to 4 serial sections (each section separated by ∼70 μm). (F) Time to occlusion in α9^fl/flLysMCre⁺ mice transfused with α9^fl/fl mice neutrophils or α9^fl/fl mice transfused with α9^fl/fl LysMCre⁺ mice neutrophils (n = 10 vessels from 5 mice/group). (G) Time to occlusion in the wild-type mice (C57BL/6J) treated with anti-integrin α9 antibody or vehicle control (n = 10 vessels from 5 mice/group). (H) Representative microphotographs of mesenteric artery thrombus in the laser-injury model (left). Mean fluorescence intensity (MFI) over time (n = 19-22 vessels from 4 mice/genotype) (right).