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C. E. Reme, K. Lang, B. Odermatt, S. Joly, M. Samardzija, K. Schwerdfeger, C. Grimm; Origin of Macrophages in Acute, Light-Induced Photoreceptor Apoptosis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2507.
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© ARVO (1962-2015); The Authors (2016-present)
Macrophages gain renewed interest in view of recent observations on genetic variants of the complement system, which dramatically increase the risk of age - related macular degeneration. Exogenous modifiers triggering inflammatory responses may further elevate the risk. Light exposure may be one of them. In acute light - damage, we observe rupture of the blood - retinal interface (BRI), release of inflammatory cytokines and macrophages in the subretinal space. We investigated the origin of macrophages in acute light - damage.
Mice: C57BL/6 were lethally irradiated (950 rad) on day 1. On day 2, 8 x 106 bone marrow (BM) cells, generated by flushing the femur and tibia of green fluorescent protein (gfp) transgenic C57BL/6 mice, were injected i.v. into recipient mice. Further, SV129/BL/6 mice were used. Light exposures: mice were exposed to 13 klux of diffuse, white fluorescent light for 2 h or to 30 mW/cm2 blue light of 410 nm ± 10 nm for 2 - 5 min. Mice recovered for various intervals before sacrifice. Morphology: eyes were enucleated and prepared for immunostaining and fluorescence microscopy. Antibodies against hematogenous and glia - derived macrophages were applied in addition to sections from gfp - positive mouse chimeras. Biochemistry: retinal mRNA and protein of MCP-1 (monocyte - chemoattractant protein - 1) were analyzed.
Immunohistochemistry indicated hematogenous origin of macrophages by positive staining for macrophage markers CD11b, CD68 and weakly for F4/80. Green fluorescent macrophages were present from 6 - 14 days after light exposure. MCP-1 mRNA significantly increased at 6, 12 and 24 h after exposure and protein at 24 and 36 h.
Our data indicate hematogenous origin of macrophages in light - damage, rupture of BRI may facilitate their attraction and migration. Contribution of activated resident microglia, as has been shown by others, needs to be further investigated. Macrophages and activated microglia may differ in their effects on apoptosis and potential immune responses.
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