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E. S. Solomon, J. C. Blanks, C. J. Dougherty, E. E. Greene, R. Tao, C. K. Dorey; IL-10 Inhibits Neovascularization in the ROP Model. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4056.
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IL-10 is essential for induction of immune privilege by antigens injected into the aqueous or vitreous. IL-10 is reported to inhibit angiogenesis induced by tumors and limb ischemia. We hypothesized that induction of IL-10 contributes to the antiangiogenic effects of intravitreally administered peptides and proteins.
Neonatal mice raised in 75% oxygen from day 7 to day 12, were given an intravitreal injection of IL-10 (1 µl of 10µg /ml) on day 12, and maintained in room air for 5 more days. Fixed eyes were cryosectioned, and every 10th section was stained with fluorescein-conjugated Griffonia simplicifolia lectin, and sequential contiguous photographs were made of each section. Morphometric analysis of retinal vascular density and area of neovascularization (NV) was performed using Metamorph.
The area of NV in IL-10 treated eyes was 924 ± 859, 80% lower than the NV area (4504 ± 1692) in contralateral untreated eyes (P<0.00004; see graph). IL-10 acted selectively on NV: it had no effect on the either the area of intraretinal blood vessels, or the percent of inner nuclear area occupied by blood vessels (P>0.5 for each). To further consider whether IL-10 acted selectively, the fraction of the total vascular area that was NV (%NV) was analyzed in each eye. IL-10 substantially reduced the %NV from 8.3 % in untreated eyes to 2.8%; P<0.006).
The potent inhibition produced by 10 ng of IL-10 -- and its half life of 2-4 hours in vivo -- indicate that the early period of retinal hypoxia may be a critical therapeutic window for prevention of neovascularization. These data raise the further possibility that endogenous production of IL-10 contributes to the antiangiogenic effect of intravitreally administered proteins. These results demonstrate that IL-10 is potent inhibitor of intravitreal, hypoxia-induced NV.
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