Figure 6 | Scientific Reports

Figure 6

From: Excess HB-EGF, which promotes VEGF signaling, leads to hydrocephalus

Figure 6

Response of cells on the ventricular surface to an EGFR ligand, HB-EGF.

(a) Confocal micrographs displaying localization of phosphorylated EGFR (P-EGFR) immunofluorescence in the striatal side of the lateral ventricles (abbreviated, V) in mice carrying human HB-EGF heterozygous (upper) and homozygous (lower) alleles at P31. These sections are co-stained with β catenin (β-cat). Note that β-cat is diffusely detected in the SVZ but not on the ventricular surface of the HB-EGF homozygote as compared to the littermate controls. V denotes lateral ventricles. Arrowhead indicates an orientation in which EGFR ligand reporter, β-gal is located near the lateral ventricles. Dashed lines indicate apical membrane of the cells on the ventricular surface. (a’) Confocal micrographs exhibiting an adjacent coronal sections stained with GFAP and Ki67 in the SVZ of mice carrying human HB-EGF heterozygous (upper) and homozygous (lower) alleles at P21. V denotes lateral ventricles. Arrowhead indicates an orientation in which EGFR ligand reporter, β-gal is located near the lateral ventricles. Dashed rectangular insets correspond to the ventricular surface shown in a. (b) Bar graphs displaying the level of immunofluorescence (IF) in P-EGFR, β catenin, DAPI and parenchymal GFAP shown in (a–a’). N = 3 in each group for all the experiments in this figure (a,b). Single (*) and double asterisks (**) represent p < 0.05 and p < 0.01, as compared to the heterozygous control, respectively, by unpaired t test (two-tailed). Scale bars, 10 μm (a) and 100 μm (a’), respectively.

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