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Fig. 6 | Molecular Neurodegeneration

Fig. 6

From: Apolipoprotein E4 impairs spontaneous blood brain barrier repair following traumatic brain injury

Fig. 6

APOE4 mice display prolonged BBB dysfunction at the NVU following TBI. (a) Immunohistochemistry analysis of lectin (inset: arrowheads = vessel, arrows = glial) and CD31 staining in the ipsilateral pericontusional cortex following TBI (n = 3–4). (b-c) Quantitative immunohistochemistry showing the expression of Claudin-5 and Zonula Occludens-1 (ZO-1) in the ipsilateral pericontusional cortex of APOE3 and APOE4 sham and injured mice. (n = 4, *p < 0.05 vs genotype sham). APOE3 and APOE4 mice were subject to TBI, before ipsilateral microvessels were isolated at 1, 3, 7 and 10 days post-injury. mRNA analysis of (d) Claudin-5 (n = 4–6, ++p < 0.01 vs relevant timepoint), (e) Zonula Occludens-1 (n = 4–6, +p < 0.05 vs relevant timepoint), (f) Occludin (n = 4–6, *p < 0.05 vs genotype sham; +p < 0.05 vs relevant timepoint) and (g) Mmp-9 (n = 4–6, ***p < 0.001, **p < 0.01, *p < 0.05, vs genotype sham. +p < 0.05, ++p < 0.01 vs relevant timepoint). All data expressed as mean ± S.E.M. Two-way ANOVA with Bonferroni post hoc test

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