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S. Sarman, M. Aronsson, A. Kvanta, I. van der Ploeg; Decreased Pathologic Retinal Neovascularization in IL–10–Deficient Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1757.
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© ARVO (1962-2015); The Authors (2016-present)
Ischemia–induced neovascularization is characterized by the presence of inflammatory cells. Earlier studies have shown the anti–inflammatory interleukin–10 (IL–10) to be anti–angiogenic. To investigate this further we have studied the degree of retinal neovascularization in IL–10–deficient and wild–type mice (C57BL/6J) in a model of oxygen induced retinopathy (OIR).
Pathologic retinal neovascularization was analyzed in a model of OIR. Seven days old mice, P7, were exposed to 75% oxygen for five days, P12, where after they were returned to normoxia for five days, P17. Animals were euthanized and the eyeballs extracted for histological analysis. Vascular nuclei above the internal limiting membrane (ILM) were counted for neovascularization. Differences between the numbers of nuclei inside the ILM were compared between IL–10–deficient (p=18) and control animals (p=20). IL–10, MMP–2, MMP–9 and VEGF mRNA levels were determined by real–time RT–PCR.
IL–10 mRNA was detected in 10% (1/10) of control mice and in 70% (7/10) of mice with OIR. Unexpectedly there was markedly decreased formation of extraretinal neovascular tufts in the IL–10–deficient mice (12 nuclei/section in IL–10–deficient mice vs 35 nuclei/section in wildtype mice). There was no significant difference between MMP–2, MMP–9 and VEGF mRNA levels in P17 IL–10–deficient mice compared to wild–type mice.
IL–10 appears to have a complex role in pathologic retinal neovascularization.
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