3K3A-APC protection against ischemic stroke in vivo requires β-arrestin 2. (A) Representative T2-weighted (structural) coronal MR scans showing postischemic injury area (hyperintense signal) in the ipsilateral cortex 24 hours after tMCAo in control and Arrb2^–/– mice on C57BL/6J genetic background treated with vehicle or 3K3A-APC (0.8 mg/kg intraperitoneally 10 minutes and 4 hours after the start of tMCAo). Postischemic injury areas are delineated by yellow dashed lines. (B-D) Injury (B), infarct (C), and edema volumes (D) 24 hours after tMCAo in control and Arrb2^–/– mice treated with vehicle or 3K3A-APC as above in panel A. Control + vehicle (n = 7); Control + 3K3A-APC (n = 6); Arrb2^–/– + vehicle (n = 7); and Arrb2^–/– + 3K3A-APC (n = 6). All volume measurements derived from structural T2-weighted MR images. Data in panels B-D are shown as dot plots representing single points per mouse. Each bar represents mean ± standard error of the mean. Statistical significance was determined by 1-way analyses of variance followed by Tukey multiple comparison test. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. ns, nonsignificant. The panels B-D in Figure 2 were modified to have the same y-axes, but the data are the same as originally submitted.