Figure S3.
Genetic deletion of VEGFR2 does not prevent CCM formation but promotes new lesion development in the forebrain in the neonatal mouse model. (A) Representative visual images and microCT renders of Cdh5-CreERT2; Krit1fl/fl; Cdh5-CreERT2; Krit1fl/fl; Kdrfl/+, and Cdh5-CreERT2; Krit1fl/fl; Kdrfl/fl mouse brains harvested on P11. Boxed regions of the right cerebrum (a–c) are shown in (a’–c’) with pair microCT renders (a’’–c’’), respectively, at higher magnification. (B) MicroCT renders of all study subjects, Cdh5-CreERT2; Krit1fl/fl; Cdh5-CreERT2; Krit1fl/fl; Kdrfl/+, and Cdh5-CreERT2; Krit1fl/fl; Kdrfl/fl mouse brains harvested on P11. The same brain specimens and corresponding microCT renders are shown in Fig. 3 M with emphasis on cerebellar lesions. Representative images in this panel highlight whole-brain and forebrain views. (C and D) microCT quantification of (C) neonatal forebrain and (D) neonatal hindbrain in Cdh5-CreERT2; Krit1fl/fl (n = 13), Cdh5-CreERT2; Krit1fl/fl; Kdrfl/+ (n = 18), and Cdh5-CreERT2; Krit1fl/fl; Kdrfl/fl (n = 8) mouse brains harvested on P11. Scale bar: 1 mm. Data shown are means ± SEM. ***P <0.001 and ****P <0.0001 by one-way ANOVA, followed by Tukey HSD post hoc test. No statistically significant (n.s.) differences are observed in (C) left: P = 0.9990; right: P = 0.1183 and (D) left: P = 0.4559; right: P = 0.9027. Tukey HSD, Tukey’s honestly significant difference. Refer to the image caption for details. The image contains multiple graphs and visual representations of mouse brains to study the effects of genetic deletion of V E G F R 2 on C C M formation. Panel A shows representative brain images and micro C T renders of C d h 5-C r e E R T 2; K r i t 1 f l slash f l; K d r genotypes highlighting lesion distribution with magnified boxed regions; Panel B shows micro C T render gallery of whole brains from all P 11 littermates displaying lesion patterns across genotypes; Panel C shows vertical bar graphs quantifying neonatal forebrain lesion volume and total forebrain volume; Panel D shows vertical bar graphs quantifying neonatal hindbrain lesion volume and total hindbrain volume. The graphs use bar plots to represent lesion volumes and total brain volumes, with statistical significance indicated by asterisks. The x-axes represent different genetic conditions, while the y-axes represent lesion volume in cubic millimeters and total brain volume in cubic millimeters. The data show significant differences in lesion volumes and total brain volumes among the different genetic conditions, with p-values indicating statistical significance.

Genetic deletion of VEGFR2 does not prevent CCM formation but promotes new lesion development in the forebrain in the neonatal mouse model. (A) Representative visual images and microCT renders of Cdh5-CreERT2; Krit1fl/fl; Cdh5-CreERT2; Krit1fl/fl; Kdrfl/+, and Cdh5-CreERT2; Krit1fl/fl; Kdrfl/fl mouse brains harvested on P11. Boxed regions of the right cerebrum (a–c) are shown in (a’–c’) with pair microCT renders (a’’–c’’), respectively, at higher magnification. (B) MicroCT renders of all study subjects, Cdh5-CreERT2; Krit1fl/fl; Cdh5-CreERT2; Krit1fl/fl; Kdrfl/+, and Cdh5-CreERT2; Krit1fl/fl; Kdrfl/fl mouse brains harvested on P11. The same brain specimens and corresponding microCT renders are shown in Fig. 3 M with emphasis on cerebellar lesions. Representative images in this panel highlight whole-brain and forebrain views. (C and D) microCT quantification of (C) neonatal forebrain and (D) neonatal hindbrain in Cdh5-CreERT2; Krit1fl/fl (n = 13), Cdh5-CreERT2; Krit1fl/fl; Kdrfl/+ (n = 18), and Cdh5-CreERT2; Krit1fl/fl; Kdrfl/fl (n = 8) mouse brains harvested on P11. Scale bar: 1 mm. Data shown are means ± SEM. ***P <0.001 and ****P <0.0001 by one-way ANOVA, followed by Tukey HSD post hoc test. No statistically significant (n.s.) differences are observed in (C) left: P = 0.9990; right: P = 0.1183 and (D) left: P = 0.4559; right: P = 0.9027. Tukey HSD, Tukey’s honestly significant difference.

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