After stroke, deletion of astrocytic CCL2 rescued several phenotypes by Slc4a4 loss, including infarct size (Figures 6B and S9A), BBB leakage (Figures 6C and 6D), increased CD31 intensity (Figures 6D and 6E), impaired tight-junctional marker expression (Claudin-5) (Figures 6D and 6F), and enhanced transcellular transport (pCav-1, Cav-1) (Figures 6D, 6G, S9B, and S9C) surrounding the peri-lesion region. Here, CCL2 is linked to stroke disorder.