Fig. 6
White matter tracts in the brain show a similar predilection to β1 integrin inhibition-induced vascular leak under hypoxic conditions. Frozen brain sections taken from mice exposed to normoxia or hypoxia (8% O2) that had received daily intraperitoneal injections of the anti-mouse β1 integrin function-blocking antibody or isotype control antibody for 4 days were stained for CD31 (AlexaFluor-488), fibrinogen (Cy-3) and DAPI (blue) (A and C) or fluoromyelin (red) and fibrinogen (AlexaFluor-488) (B and D). A-B and C-D images show the cerebellum and cerebral cortex/corpus callosum, respectively. Scale bars = 500 μm. White dotted line demarcates the WM corpus callosum (inside) from the surrounding grey matter. E-F. Quantification of the number of vascular leaks/unit area in the cerebellum (E) or cerebral cortex/corpus callosum areas after 0- or 4-days hypoxia. Results are expressed as the mean ± SEM (n = 6–10 mice/group). *** p < 0.001. Note that under hypoxic conditions, β1 integrin inhibition greatly increased the extent of vascular disruption in the brain, preferentially in the cerebellar and corpus callosum WM tracts