Figure S2.
TIE2 phosphorylation is unaffected by craniotomy, stereotactic injection, and AAV transduction, while VEGFR2 deletion fails to prevent CCM formation in the adult mouse model. (A) Ai14 mice between age 8–10 wk underwent craniotomy and received AAV-Cre injections to induce focal Cre-mediated tdTomato reporter expression in the cerebral cortex below a cranial window. Representative images showing immunostaining for CD31, TIE2, and pTIE2, with DAPI counterstaining in brains harvested on POD 7. (B) Quantification of MFI of pTIE2Y992 normalized to total TIE2, compared with tdTomato-negative contralateral brain regions that received no procedure or AAV-Cre administration. A total of three mice in each group were measured and quantified. Data shown are means ± SEM. No statistically significant (n.s.) differences are observed (P = 0.1730) by unpaired two-tailed Welch t test. Scale bar: 100 μm. (C) MicroCT renders of all study subjects, including seven Krit1fl/fl; iPik3caH1047R and seven Krit1fl/fl; iPik3caH1047R; Kdrfl/fl mouse brains, harvested on POD 21. Two pairs of representative microCT renders from this complete cohort are presented in Fig. 3 E with the corresponding brain specimens to demonstrate genotype-dependent differences in lesion burden. (D) Representative images showing H&E and Prussian blue staining of Krit1fl/fl; iPik3caH1047R and Krit1fl/fl; iPik3caH1047R; Kdrfl/fl mouse brains harvested on POD 21. Refer to the image caption for details. Panel A shows immunostaining images of A i 14 mouse brains with markers for C D 31, T I E 2, p T I E 2, and DAPI counterstaining. The images are divided into two rows: the top row shows the ipsilateral side with t d Tomato expression, while the bottom row shows the contralateral side. Panel B presents a vetical bar graph quantifying the mean fluorescence intensity of p T I E 2 Y 992 normalized to total T I E 2, comparing t d Tomato-positive and t d Tomato-negative regions. Panel C displays micro C T renders of mouse brains from different genotypes, highlighting lesion formation. Panel D includes representative images of hematoxylin and eosin and Prussian Blue staining of mouse brains, illustrating tissue structure and iron accumulation.

TIE2 phosphorylation is unaffected by craniotomy, stereotactic injection, and AAV transduction, while VEGFR2 deletion fails to prevent CCM formation in the adult mouse model. (A) Ai14 mice between age 8–10 wk underwent craniotomy and received AAV-Cre injections to induce focal Cre-mediated tdTomato reporter expression in the cerebral cortex below a cranial window. Representative images showing immunostaining for CD31, TIE2, and pTIE2, with DAPI counterstaining in brains harvested on POD 7. (B) Quantification of MFI of pTIE2Y992 normalized to total TIE2, compared with tdTomato-negative contralateral brain regions that received no procedure or AAV-Cre administration. A total of three mice in each group were measured and quantified. Data shown are means ± SEM. No statistically significant (n.s.) differences are observed (P = 0.1730) by unpaired two-tailed Welch t test. Scale bar: 100 μm. (C) MicroCT renders of all study subjects, including seven Krit1fl/fl; iPik3caH1047R and seven Krit1fl/fl; iPik3caH1047R; Kdrfl/fl mouse brains, harvested on POD 21. Two pairs of representative microCT renders from this complete cohort are presented in Fig. 3 E with the corresponding brain specimens to demonstrate genotype-dependent differences in lesion burden. (D) Representative images showing H&E and Prussian blue staining of Krit1fl/fl; iPik3caH1047R and Krit1fl/fl; iPik3caH1047R; Kdrfl/fl mouse brains harvested on POD 21.

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