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Jason M. Butler, Steven M. Guthrie, Mehmet Koc, Aqeela Afzal, Sergio Caballero, H. Logan Brooks, Robert N. Mames, Mark S. Segal, Maria B. Grant, Edward W. Scott
Published in Volume 115, Issue 1
J Clin Invest. 2005; 115(1):86–93 doi:10.1172/JCI22869
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Figure 6

Anti–SDF-1 antibody prevents retinal neovascularization by HSC-derived circulating endothelial progenitors. All micrographs are merged confocal images of retinal flat mounts. Animals were perfused with a red fluorescent dye (RITC-dextran; Sigma-Aldrich) to delineate the vasculature. New blood vessels incorporate GFP+ HSC progeny, thereby forming areas of green/yellow fluorescence. Model control: Right, or treated, eyes from 4 representative C57BL/6.gfp animals in which retinal ischemia was induced according to our standard model. GFP+ progeny suggestive of astrocytes or glia are also seen incorporated outside of the vasculature. Negative control: Left, or untreated, eyes of the same 4 C57BL/6.gfp mice in which retinal ischemia was induced according to our standard model in their right eyes. Note the lack of recruitment and incorporation of transplanted gfp+ HSC progeny. Mock injections: Right, or treated, eyes from 4 representative C57BL/6.gfp mice in which retinal ischemia was induced according to our standard model with the added step of intravitreal injection with PBS containing an isotype control antibody to a final concentration of 1 μg/μl. Note the similar recruitment and incorporation of transplanted GFP+ HSC, as in model control. Anti–SDF-1, 1×, 4 injections: Right, or treated, eyes from 4 representative C57BL/6.gfp mice in which retinal ischemia was induced according to our standard model with the added step of intravitreal injection with PBS containing an anti–SDF-1 antibody to a final concentration of 1 μg/μl. Note the absence of newly formed GFP+ HSC in the vascular tufts.