Fig. 1
β1 integrin inhibition greatly increases hypoxia-induced spinal cord vascular disruption, preferentially in WM. Frozen spinal cord 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) and fibrinogen (Cy-3) (A), fluoromyelin (red) and fibrinogen (AlexaFluor-488) (D), or CD31 (AlexaFluor-488), fibrinogen (Cy-5), or TER-119 (Cy-3) (E). Scale bars = 500 μm, except for high power (HP) images in lower panel of A, where scale bar = 200 μm. White dotted line demarcates the GM (inside) from the WM (outside). (B-C) Quantification of the total area (B) or number of vascular leaks/FOV (C) in the spinal cord after normoxia or 4-days hypoxia. Results are expressed as the mean ± SEM (n = 6–10 mice/group). *** p < 0.001. Note that β1 integrin inhibition greatly increased the extent of hypoxia-induced vascular disruption in the spinal cord, preferentially in the WM