The modulation of EPC homing to ischemic tissue by sE-selectin. (A) Representative figure showing more EPCs attached to E-selectin–adsorbed gelatin plate (E-sel) than BSA-adsorbed plate (BSA, control protein). Pretreatment with blocking antibody against E-selectin (anti–E-selectin Ab) significantly attenuated EPC attachment to the E-selectin–adsorbed plate. Quantitative analysis of attached EPCs (†P < .05; n = 4, respectively; scale bar, 500 μm). (B) Representative fluorescent images of muscle 1 week after ischemia (scale bar, 100 μm). One million EPCs cultured from eGFP transgenic mice (green) were “systemically administered” to WT and E-sel^−/− mice after induction of ischemic hindlimb. Before EPC transplantation, either control antibody or anti–E-selectin antibody was injected into WT mice intravenously. In E-sel^−/− mice, BSA or sE-selectin (sE-sel) was locally injected into the ischemic muscle. BS-1 lectin staining (red) was used for visualizing ECs. Dual-positive cells were the differentiated ECs from donor EPCs. They were less observed in anti–E-selectin antibody group of WT mice than in control antibody group. In E-sel^−/− mice, sE-selectin treatment increased dual-positive cells compared with BSA treatment. (C) Quantitative analysis of incorporated EPCs to ischemic limb. The number of EPCs homing to ischemic limb decreased by blocking E-selectin in WT mice (†P < .05; n = 4, respectively) and increased by injecting sE-selectin in E-sel^−/− mice (†P < .05; n = 4, respectively). Error bars in panels A and C represent SD.