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J.-L. Bourges, J.-M. Ortiz Egea, M.-C. Naud, N. Minet, M. Berdugo-Polack, L. Leconte, L.-M. Bachelot, F. F. Behar-Cohen; Inhibition of Corneal Neovascularization With a New Antiangiogenic Recombinant Protein. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2809.
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to inhibit proliferation of new vessels growing across cornea with a novel antiangiogenic recombinant 55 kDa protein NOV (Sisene, France) and its C terminal truncation 26.4 kDA NOVCter (Sisene, France).
New vessels were induced on Lewis rat corneas by intralamellar insertion of 0.2 mm elevax implant loaded with LPS (Sigma-Aldricht, France). Implanted rats were randomly assigned to the following subconjunctival treatment (10 µl/injection) groups NOV1 and NOV2 respectively receiving 1 and 2 µg of native NOV protein (n=5 and 7 eyes), NOVCter receiving 2 µg of native NOVCter protein (n=6 eyes), and PBS control (n=8 eyes). New vessels were quantified after 6 and 8 days on pictures by two masked observators grading (0 to 3) vessels’density, diameter and spreading. After sacrifice at D8, corneas were stained with lectin and further analyzed with confocal microscope.
At D8, the mean total scores ±SD for density, diameter and vessels’ speading area were were respectively 2.66±0.5, 2.66±0.5and 2.8±0.4 for the PBS group, 2.36±0.8, 2.8±0.4, 2.27±0.8 and 1.9±0.8, 1.8±0.9, 2.1±0.7 for NOV1 and NOV2 and 2.27±0.8, 2.27±0.8, 2.27±0.9 for NOVCter. Vessels growing on corneas from group NOV2 were significantly reduced versus PBS (P<0.001). Clinical observations were confirmed with 3D concofal microscope examination.
Recombinant NOV protein is a promising treatment to limit induced neovascularization. A dose effect is observed and might explain NOVCter results
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