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. 2011 Apr;3(4):235–245. doi: 10.1002/emmm.201100126

Figure 5. Inhibition of CNV using barrier modulation.

Figure 5

  1. Mice perfused with FITC-dextran-200 (FD-200) prior to preparation of choroidal flatmounts, displayed poorly perfused lesions (green) at the site of the laser burn when compared to the density of endothelial cells in the region stained with isolectin-Alex 568 (red).
  2. C57/Bl6 mice were administered NT AAV-2/9 in their left eye and CLDN5 AAV-2/9 in their right eye with doxycycline supplementation (2 mg/ml) in their drinking water for 3 weeks. CNV was induced with a targeted laser burn (140 mW, 100 mS, 50 µm spot size) in either the NT AAV-2/9 or CLDN5 AAV-2/9 injected eye and 4 days post-laser burn, mice were injected with 31.25 mg/kg 17-AAG i.p. Mice were injected again 4 days later. CNV volumes in the eyes of mice receiving the CLND5 AAV-2/9 were significantly reduced when compared to the NT AAV-2/9 injected eyes (*p = 0.0189).
  3. CNV formation in mice inoculated sub-retinally with CLDN5 AAV-2/9 were shown to be consistently reduced when compared to the NT AAV-injected eyes (n = 5–7 mice per experimental group).
  4. 17-AAG is a potent inhibitor of VEGFR-2 expression via the inhibition of hsp-90.
  5. In the same manner as described above, mice were injected with 20 mg/kg Sunitinib malate (Sutent®) i.p. on days 4 and 8 post-laser burn and CNV volumes were shown to be significantly reduced in CLDN5 AAV-2/9-injected mice compared to NT AAV-2/9 controls (*p = 0.0393).
  6. Again, confocal Z-stack images showed consistently decreased CNV volumes in the CLDN5 AAV-2/9-injected eyes compared to the NT AAV-2/9-injected eyes.