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Miho Nozaki, Eiji Sakurai, Brian J. Raisler, Judit Z. Baffi, Jassir Witta, Yuichiro Ogura, Rolf A. Brekken, E. Helene Sage, Balamurali K. Ambati, Jayakrishna Ambati
Published in Volume 116, Issue 2
J Clin Invest. 2006; 116(2):422–429 doi:10.1172/JCI26316
Abstract | Full text | PDF
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Figure 1

VEGFR-1 ligands suppressed CNV. (A) Stacked confocal image of representative laser-induced CNV lesions in PBS-treated eyes were larger than in VEGF-A–treated (0.29 pmol) or PlGF-1–treated (4.3 pmol) eyes and smaller than in VEGF-E–treated (0.34 pmol) eyes. Scale bars: 100 μm. (B) PBS treatment alone did not reduce CNV, and VEGF-A (0.1 pmol) reduced CNV regardless of the treatment of the fellow eye. n = 15–46 per data point. #P < 0.05 compared with corresponding uninjected or PBS-treated groups. (C) VEGF-A (red; n = 38–46 per data point) and PlGF-1 (blue; n = 18 per data point) reduced CNV at 1 week after injury in a dose-dependent fashion. VEGF-E (purple) and PlGF-1 together (single data point depicted as dotted line) suppressed CNV similar to PlGF-1 alone. n = 12 per data point. VEGF-E increased CNV. n = 12. *P < 0.01, #P < 0.05 compared with PBS; §P < 0.01 compared with VEGF-E; P > 0.90 compared with PlGF-1. (D) CNV inhibited by CoCl2 (0.77 nmol) was abrogated by anti–VEGF-A antibody (6.7 fmol) but not by control goat IgG (6.7 fmol). Anti–VEGF-A antibody modestly reduced CNV compared with goat IgG. *P < 0.01 compared with control (PBS). #P < 0.05 compared with goat IgG. n = 18–24 per data point.