Loss of SPARC-mediated VEGFR-1 suppression after injury reveals a novel antiangiogenic activity of VEGF-A
J. Clin. Invest. Miho Nozaki, et al. 116:422 doi:10.1172/JCI26316 [
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Figure 1VEGFR-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 CoCl
2 (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.
