FIGURE 5.

Immunohistochemical analysis of changes in the production of cell-type-specific markers in the brain of transgenic mice after FCI. (A) Representative images of the SVZ isolated from CTRL and MCAO mice without Wnt pathway modulation. Increased stainings of neuroblasts marked by doublecortin (DCX), glial fibrillary acidic protein (GFAP)-positive astrocytes, and dividing cells harboring proliferating cell nuclear antigen (PCNA) were recorded 3 days after the induction of ischemia. Scale bar = 0.2 mm. Modulation of the canonical Wnt signaling pathway changed the incidence of cell types under control, physiological conditions (CTRL) as well as 3 days upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Diagrams show quantification of immunohistochemical staining in the SVZ of CTRL and MCAO mice only treated with either tamoxifen (TAM) or vehicle, corn oil (CO). Tamoxifen-induced production of dominant negative human T-cell factor protein (dnTCF4; B) and Dickkopf 1 Wnt inhibitory protein (Dkk1; C) were used to achieve Wnt signaling inhibition and, conversely, production of constitutively active β-catenin (Ex3; D) was initiated in order to obtain Wnt pathway activation. Experiments were performed using two biological replicates and three technical replicates for each treatment (n = 6). Average values of the control mice (CTRL CO) were arbitrary set to 100% of immunogenic signal. Error bars represent standard deviation and one-way ANOVA was used to determine significant differences among the experimental groups; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Ex3, exon 3.