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Judit Z. Baffi, Yoshio Hirano, Hiroki Kaneko, Kiyoshi Yamada, Miho Nozaki, Atsunobu Takeda, Jayakrishna Ambati; CCR3 and MCP-1 Ablation Inhibits Laser-induced Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1010.
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© ARVO (1962-2015); The Authors (2016-present)
To compare the effect of the targeted disruption of chemokine receptor 3 (CCR3), monocyte chemotactic factor-1 (MCP-1), or both genes in the development of choroidal neovascularization (CNV).
Laser photocoagulation was used to induce CNV in CCR3 knockout, MCP-1 knockout, CCR3 x MCP-1 double knockout, and wild-type C57BL/6J mice. CNV responses were compared on the basis of en masse volumetric measurements obtained by confocal microscopy and fluorescein angiography 1 week after laser injury.
Significantly fewer lesions exhibited fluorescein leakage defined to be pathologically significant in CCR3 and MCP-1-deficient mice at week 1 compared with wild-type mice. There were a greater number of lesions without fluorescein leakage in CCR3-MCP-1 double knockout mice than in the other two groups at the same time point. The volume of CNV in CCR3- and MCP-1 deficient mice was significantly less than in wild type, and further suppressed in CCR3-MCP-1 double knockout mice.
These data suggest non-overlapping roles of MCP-1 and CCR3 in the development of CNV that could be therapeutically exploited.
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