Fig. 1.
Continuous presence of autocrine VEGF is required for endothelial cell survival. (A) H&E-stained histological sections of VEGF-ECKO mice after hypoxia treatment. Arrowheads indicate areas of hemorrhage. Brackets indicate thickness of outer intestinal wall. (B) Quantification of A showing average number of lesions per VEGF-ECKO mouse under conditions of normoxia or hypoxia. No lesions were observed in control mice (VEGF-ECKO: n=14 normoxia, n=10 hypoxia; Control: n=9 normoxia, n=10 hypoxia). (C) Survival analysis of iVEGF-ECKO mice after tamoxifen injection at 10 weeks. Sudden death starting 15 weeks post-injection (Control n=25, iVEGF-ECKO n=30). (D) Viability of endothelium isolated from the liver of adult floxed-VEGF mice treated in culture with adenoviral GFP (Ad-GFP) or Cre (Ad-Cre) (n=6). (E) siRNA targeting VEGF results in a more than 50% decrease of VEGF transcript (n=3). (F) KD-VEGF reduces cell viability. Images were collected from the cell layer 5 days after the first transfection. Scale bar, 100 μm. (G) Quantification of cell confluence from F (n=4). For all graphs, error bars indicate the mean±s.d.; *P<0.05, **P<0.005.