Fig. 3
β1 integrin blockade does not prevent hypoxia-induced endothelial proliferation or increased vascularity in young or aged brain. Frozen brain sections taken from young (8–10 weeks) and aged (20 months) 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 the proliferation marker Ki67 (Cy-3). Images show the midbrain in young (A) or aged (B) mice. Scale bar = 200 μm. C–F. Quantification of the number of proliferating endothelial cells (CD31 + /Ki67 + cells)/FOV (C–D), or vascular area (% of total) (E–F) after 0- or 4-days hypoxia. Results are expressed as the mean ± SEM (n = 6–7 mice/group). *p < 0.05. Note that β1 integrin blockade greatly did not prevent hypoxia-induced endothelial proliferation or increased vascularity, and unexpectedly, increased hypoxia-induced endothelial proliferation in young brain. OB olfactory bulb, MB midbrain, ST striatum, CX cerebral cortex, CC corpus callosum