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. 2002 Apr 1;157(1):149–160. doi: 10.1083/jcb.200109079

Figure 7.

Figure 7.

VEGF-induced VP defect in integrin β5–deficient mice. (A) The VEGF-induced VP response in the dermis of β5−/−, β3−/−, or control mice was determined by intradermal injection of VEGF (400 ng) into mice that had been previously injected with EB, a fluorescent VP indicator. The extravasation of EB from the blood vessels was quantitated by fluorimetry (O.D.600), as previously described (Eliceiri et al., 1999). (n = 7) (*, P < 0.05) (B) The VEGF-induced VP response in cerebral blood vessels was identified by the extravasation of EB from β5−/− or control mice that had been stereotactically injected with VEGF or saline, as previously described (Eliceiri et al., 1999; Paul et al., 2001). Laser confocal scanning microscopy was used to visualize the fluorescence of the extravasated EB in representative brain cross sections. Bar, 100 μm. (C) Infarct volumes following cerebral ischemia were determined in TTC-stained coronal sections of β5−/− or control mice, as previously described (Paul et al., 2001). Quantitation of the infarct volumes was measured as previously described (Paul et al., 2001) (P < 0.02) (left). Representative micrographs of TTC-stained brain sections reveal the zone of VEGF-mediated neuronal damage (right). Bar, 2 mm.