AKAP12 KO mice showed an impaired fibrotic scar structure with loss of junction complexes.

<p>(A) The structure of the scar tissue was unstable in the AKAP12 KO mice (a/d). More IBA1-positive immune cells infiltrated across the fibrotic scar in the AKAP12 KO mice (b/e). AKAP12 KO mice showed much more hypertrophic GFAP-positive astrocytes and IBA1-positive microglial cells near the fibrotic scar (c/f). Scale bar: 200 µm (left panel), 40 µm (right panel) (B) The expression of junction proteins in the fibrotic scar was reduced in the AKAP12 KO mice compared to the WT mice on day 21 after injury. Brain sections were stained with antibodies against ZO-1, Occludin, and E-cadherin. The lower three columns are magnified images of the fibrotic scar. Scale bar: 200 µm (upper panel), 40 µm (lower panel) (C) The experimental condition was same for panel b. For each marker, the immunoflouresence intensity of three representative slides per mouse were analyzed using Image J. (Mean ± S.D.; n = 4 mice per each time; P#<0.001) (D) The global level of junction proteins were decreased in the AKAP12 KO mice. The lesion tissues were harvested from the brains of mice on day 21 after injury and the tissue lysates were analyzed by Western blot (Mean ± S.D.; n = 4 mice per WT and KO; P*<0.05, P**<0.01). [LC: lesion core, FS: fibrotic scar, GS: glial scar].