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. 2005 Mar 2;25(9):2366–2375. doi: 10.1523/JNEUROSCI.5071-04.2005

Figure 3.

Figure 3.

eNOS-deficient mice exhibit reduced angiogenesis after stroke. Angiogenesis was indicated by BrdU-immunoreactive endothelial cells, vascular density, and perimeter in the ischemic border at 7 d after stroke. A, B, BrdU immunoreactivity in the ischemic border in wild-type (WT) control MCAo mice (A) and in eNOS-/- MCAo mice (B). D, E, vWF immunoreactivity vessels in the ischemic boundary area in wild-type mice (D) and eNOS-/- mice (E).C, F, G, Quantitative data that eNOS-deficient mice significantly (p < 0.05) decrease the number of BrdU-immunoreactive cells in vessels (C), vascular perimeter (F), and density (G) in the ipsilateral hemisphere compared with wild-type control MCAo. *p < 0.05 compared with wild-type MCAo control. H-J, TERT immunostaining in the ischemic border in wild-type mice (H) and eNOS-/- mice (I). J, Quantitative data that eNOS-deficient mice significantly (p < 0.05) decrease the number of TERT-immunoreactive cells in vessels in the ipsilateral hemisphere compared with wild-type control MCAo. K, Corneal angiogenesis assay in control wild-type mice. L, M, Corneal angiogenesis assay treated with VEGF in wild-type mice (L) and eNOS-/- mice (M), respectively. N, Quantitative data that eNOS-deficient mice significantly (p < 0.05) reduce VEGF-induced angiogenesis in the cornea compared with wild-type mice treated with VEGF. Scale bars: B, E, 100 μm; I, 50 μm.