Erythropoietin (EPO) mobilizes bone marrow cells with an EPC phenotype that are recruited to the sites of neovascularization but are not incorporated in the neovessels. (A) Flow chart of the experimental procedure. Sex-mismatched AAV-VEGF–treated mice that received a transplant were treated with EPO in order to mobilize endothelial progenitor cells from the bone marrow. (B) Flow cytometry analysis of mononuclear cells from peripheral blood and spleen. Animals treated with EPO (but not those injected with AAV-VEGF or AAV-LacZ) showed a significant increase of Flk-1⁺ and Flk-1⁺/CD34⁺ cell populations, indicative of the mobilization of endothelial progenitors. Data (mean ± SD from 10 animals per group) represent the percentage of positive cells in the population of light scatter dot plots of monocyte-sized cells (see also Figure S2 and Asahara et al⁸ ). NS indicates not significant. (C) Immuno-FISH analysis of VEGF-treated muscle sections of animals treated with EPO. Despite the mobilization of EPCs, there was no increase in the number of Y-chromosome–positive cells expressing the CD31 endothelial markers at the sites of VEGF-induced neovascularization. Red indicates CD31⁺ cells; green, Y chromosome; and blue, nuclei stained with DAPI.