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. 2013 Apr 16;8(4):e61831. doi: 10.1371/journal.pone.0061831

Figure 2. The failed therapeutic neovascularization after VEGF-A overexpression in the early stage (7 day) of mouse hindlimb ischemia model.

Figure 2

(A) Laser Doppler Imaging (LDI) measured after right femoral artery ligation and at d7. (B) Quantification of LDI (ischemic versus non-ischemic hindlimb) revealed no significant neovascularization by VEGF-A at low (rAAV.lVEGF-A) or high doses (rAAV.hVEGF-A), but deterioration of perfusion in the rAAV.hVEGF-A+Ang2 group compared vehicle group (#P<0.05, vs. vehicle). (C) Fluorescence microscopy images of gastrocnemius muscle sections from control (rAAV.LacZ) or ischemic hind limb co-stained with DAPI (blue, nucleus), anti-NG2 (green, pericyte) antibody and anti-PECAM-1 (red, endothelial cell) antibody at d 7 after ligation. (D) Quantitative evaluation of capillary/muscle fibre ratio (CMF-R) demonstrated the ability of high VEGF-A with or without Ang2 to induce capillary growth in vivo. (E) Pericyte coverage was unaffected by lVEGF-A, but reduced in hVEGF-Agroup compared to vehicle group and even further reduced through the co-application of rAAV.Ang2. (MEAN ± SEM, n = 7,* p<0.05, ** p<0.01).