Fig. 1: Pdcd10BECKO mice develop CCM lesions but survive to adulthood. | Nature Communications

Fig. 1: Pdcd10BECKO mice develop CCM lesions but survive to adulthood.

From: Caveolae-mediated Tie2 signaling contributes to CCM pathogenesis in a brain endothelial cell-specific Pdcd10-deficient mouse model

Fig. 1: Pdcd10BECKO mice develop CCM lesions but survive to adulthood.

ac CCM lesion quantification in WT, Pdcd10BECKO, and Pdcd10ECKO mice at P10. Representative images of H&E staining and lesion quantifications in the cerebrum (arrows) and cerebellum (asterisks) are shown. The numbers of total lesions and lesions with different sizes were quantified as # of lesions per 10 coronal sections, which were 100 μm apart. n = 10 mice per group. d Cumulative survival curve for WT (Pdcd10fl/fl), Pdcd10BECKO (Mfsd2aCreERT2; Pdcd10fl/fl), and Pdcd10ECKO mice (Cdh5-CreERT2; Pdcd10fl/fl). N for each group is indicated. P < 0.0001 (Log-rank test). e Brain/body-weight ratios. Brain weight, body weight, and the brain/body-weight ratios are presented for WT and Pdcd10BECKO mice at 6–9 months old. n = 3 mice per group. fk CCM lesion characterization and quantification in WT and Pdcd10BECKO at 2–6 months. Representative images of fresh tissues, H&E staining (lesions indicated by asterisks), iron deposits (blue patches identified by Prussian blue), collagen deposition (red patches identified by Sirius Red), and EC proliferation (Ki67+) in the cerebrum (f, g) and cerebellum (h, i). Arrows indicate positive staining. The numbers of total lesions and lesions with different sizes were quantified as # of lesions per 10 coronal sections, which were 200 μm apart. n = 10 mice per group. Data are means ± SEM. P values are indicated, two-way ANOVA followed by Sidak’s multiple comparisons test (b, c, e, j, k). Scale bars: 25 μm (a); 100 μm (g, i); 1 mm (f, h). Source data are provided as a Source data file.

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