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. 2004 Jun 21;101(26):9833–9838. doi: 10.1073/pnas.0400337101

Fig. 3.

Fig. 3.

Vessel remodeling after brain trauma. (A) Density of vessels in the area surrounding the lesion significantly increases in control as well as in LID mice (***, P < 0.001; n = 4 animals per group). (B Left) Fluorescence photomicrographs of the perilesion site (arrow) in LID mice showing IGF-I immunoreactive cells. The majority of the IGF-I+ cells are astrocytes (GFAP+) as determined by confocal analysis (Merge). Control littermate mice show an identical local IGF-I response. (Bars = 50 μm.) (Right) Neovascularization is restricted to the perilesioned area as determined by lectin staining of brain vessels. The arrow indicates the cannula tract (14 days after injury). Note the heavy lectin staining concentrated around the lesion area. (Scale bar = 100 μm.) (C) Levels of HIF-1α increase 3 days after injury in the perilesion area in both groups, although in LID mice, the increase is smaller. The upper gel shows a representative HIF-1α blot, and the lower gel shows the control of protein load with anti-PI3K. Histograms show densitometric quantitation of HIF-1α (***, P < 0.001 vs. sham-injured mice; n = 4). (D) Levels of VEGF around the lesion area increase 3 days after injury in both experimental groups. The upper gel shows a representative VEGF blot, and the lower gel shows the control of protein load. Histograms show quantitation of VEGF (**, P < 0.01 vs. sham mice; n = 4).