Figure 7
PUR promotes regeneration after stroke. Expression of GAP43 in the ischemic zone of (a) VEH- and (b) PUR-treated animals at 14 d after stroke. GAP43+ cells with neuroblast morphology (arrows). (c) DCX+ (arrow heads) and GAP43/DCX+ (arrows) cells in the ischemic cortex of PUR-treated animals. (d) Quantitative analysis of GAP43, DCX and GAP43/DCX+ cells. Cells were counted in eight 300 × 300 μm2 squares in the ischemic area. Data are the mean±S.E.M. of n=8–10; **P<0.01. (e) DCX+ cells form clusters (arrow) and chains (arrowhead) of migrating neuroblasts in the CC. (f) DCX+ cells (arrowhead) found to detach and migrate from SVZ toward the ischemic area. (g) DCX+ cells migrate along blood vessels. (h) Immunoblot for GFAP, GAP43, synaptophysin and β-actin at 14 d after MCAO. Representative blots of n=4. (i) Quantification of protein levels relative to loading control β-actin. Data are the means of n=4±S.E.M.; *P<0.05. Expression of synaptophysin in the peri-infarct area of (j) VEH- and (k) PUR-treated animals. (l) Newly generated endothelial cells found in the penumbra (arrow). (m) Neovascularization in the infarct area. Bromodeoxyuridine (BrdU)/CD31 labels endothelial cells generated between 4 and 7 d after MCAO (arrows). (n) Newly generated endothelial cells as part of large size vessels in the infarct area. (o) Quantitative analysis of vascular density (CD31+ vessels) and newly generated (BrdU/CD31+) endothelial cells found in the penumbra and ischemic core at 14 d after stroke. Vascular density and endothelial cell numbers were analyzed in two 300 × 300 μm2 squares placed in the peri-infarct or infarct cortex. Data are the means of n=5–7±S.E.M. (p) Quantitative analysis of BrdU+, Olig2+ and BrdU/Olig2+ cells. Cells were counted in three 300 × 300 μm2 squares in the peri-infarct area of VEH- and PUR-treated animals. Data are the mean±S.E.M.; n=5–7. Scale bar, 50 μm for (a–c, e, f, j, k and m) 20 μm for (g and l) N. CP, caudate putamen; Cx, cortex; LV, lateral ventricle
