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Shuichiro Hirahara, Miho Nozaki, Masaharu Ohbayashi, Norio Hasegawa, Daisuke Ozone, Yuichiro Ogura; Suppression of Retinal Neovascularization by Anti-CCR3 Treatment for Oxygen Induced Retinopathy Model in Mice. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5402.
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To investigate the association between retinal neovascularization and CCR3 and to evaluate the efficacy of anti-CCR3 treatment for retinal neovascularization in mice model of oxygen induced retinopathy (OIR).
Retinal neovascularization model was obtained by OIR model in C57BL/6J mice. The anti-CCR3 antibody was injected into vitreous humor at postnatal day12, when the pups were taken out from the oxygen chamber. The area of capillary non-perfusion was measured by retinal whole mount. ELISA was performed to evaluate the chronological change of CCL11 (eotaxin) expression in retina. Real-time RT-PCR for CCR3 expression in the retina, and immunohistochemistry for CCR3, CCL11,CD31 and Ki67 was examined.
Intravitreous injection of anti-CCR3 antibody significantly suppressed the area of capillary non-perfusion (p<0.05) in retina of OIR model mice. The mean CCL11 protein level was temporally decreased under hyperoxia (p<0.05).In the retina of OIR, the CCL11 level began to rise at postnatal day14, significantly increased at postnatal day17 (P17) (p<0.05). CCR3 mRNA expression was significantly upregulated in P17 OIR murine retina. Intravitreous injection of anti-CCR3 antibody appeared to suppress CCR3, CCL11 and Ki67 expression in retina of OIR model mice.
There was correlation between retinal neovascularization between CCR3 and retinal neovascularization. The present data suggest that the anti-CCR3 treatment can suppress retinal neovascularization. Although our findings may warrant further investigation, anti-CCR3 treatment may have potential as a new therapy for proliferative retinopathy such as diabetic retinopathy and retinopathy of prematurity.
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