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K. Yamada, M. Nozaki, S. Yamasaki, J. Z. Baffi, A. Takeda, M. Kleinman, M. Mack, Y. Ogura, E. Sakurai, J. Ambati; CCR2-Independent MCP-1 Driven Angiogenesis in Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2358.
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© ARVO (1962-2015); The Authors (2016-present)
Monocyte chemoattractant protein-1 (MCP-1) and its only known receptor CCR-2 control macrophage mobilization in vivo. We probed the existence of CCR2-independent MCP-1-driven responses in the laser injury induced model of choroidal neovascularization in mice.
CNV was induced by laser injury and volumes measured 7 or 14 days later by confocal evaluation of Isolectin B4 staining of RPE-choroid flatmounts. Neutralizing antibodies (Ab) against MCP-1 or CCR2, control IgGs, and recombinant MCP-1 were injected into the vitreous following injury.
CNV volume was inhibited to a greater extent in MCP-1-/- mice (77±5%) than in CCR2-/- mice (77±5%; P=0.05). MCP-1 nAb reduced CNV (64±3%) to a greater extent (53±5%; P=0.01) than CCR2 nAb in wild-type mice. Recombinant MCP-1 administration increased CNV volume in CCR2-/- mice to supra-baseline levels in dose-dependent and pertussin-toxin sensitive fashions. MCP-1 nAb reduced CNV size in CCR2-/- mice but CCR2 nAb did not reduce CNV size in MCP-1-/- mice.
These findings point to the existence of a novel CCR2-independent Gi-protein coupled receptor that transduces MCP-1 signaling.
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