Fig. 2ABrain lesions that resemble CCM are present in aged
ANKS1A KO mice. (A) In the neocortex of aged
ANKS1A-deficient mice, representative fluorescent images show erythrocyte leakage associated with CCM-like vessel lesions. In our experiments, we used mice that are older than 16 months of age (scale bar, 10 μm). The mean intensity of hemoglobin staining in the WT group was set to 1. The data were quantified and presented as means±SD (N=3 mice per each group, n=8 sections). Orthogonal projection images of the CCM-like lesion shown in
. The arrows mark erythrocytes leaking into the dilated focal cavity surrounding the CCM-like lesion (scale bars, 10 μm). (B) A similar immunohistochemical staining process was performed as described in panel A, with the exception that the images show erythrocyte leakage in the subventricular zone of the aged mice lacking
ANKS1A (scale bar, 20 μm). The data were quantified and presented as means±SD (N=3 mice per each group, n=8 sections). (C) The images show immunoglobulin G-positive staining in the neocortex of aged
ANKS1A-deficient mice (scale bar, 10 μm). The white arrow indicate that the IgG-positive structures are matched with the DAPI-positive cells (scale bar, 10 μm). The microscopic filed containing CCM-like lesions was used for quantification. The data were quantified and presented as means±SD (N=3 mice per each group, n=8 sections). (D) A representative fluorescence image of Evans blue extravasation in the neocortex of aged
ANKS1A-deficient mice (scale bar, 20 μm). An illustration showing that focal cavitation forms in adjacent sections due to the CCM-like lesion (right and top panel). The data were quantified and presented as means±SD (N=3 per group, n=18 sections).
