Fig. 2From: Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitmentEvaluation of characteristics and functionalities of EPCs. a After isolation of EPCs from wild-type (WT) and Lnk-deficient mice, EPC surface markers, including Sca-1, c-Kit, CD34, and Flk-1, were analyzed on a FACS. b The graph shows the percentage of EPCs with surface markers among WT and Lnk-deficient EPCs. Values are mean ± SEM; ** p < 0.01 compared to WT EPCs. c Proliferation of EPCs was evaluated in serum-free or complete media by a 5-bromo-2′-deoxyuridine (BrdU) assay. Values are mean ± SEM; ** p < 0.01 compared to proliferation of WT EPC in a serum-free medium; ## p < 0.01 compared to WT EPCs. d Tube formation capacity of HUVECs, WT EPCs, and Lnk-deficient EPCs was determined by a Matrigel tube formation assay (magnification × 40). e The graph shows the number of capillaries among HUVECs, WT EPCs, and Lnk-deficient EPCs. Values are mean ± SEM; ** p < 0.01 compared to HUVECs and ## p < 0.01 compared to WT EPCs. f Migration capacity was assessed by a wound scratch assay (magnification × 40). g The graph shows the number of migrating cells among WT EPCs and Lnk-deficient EPCs in response to VEGF or SDF-1α. Values are mean ± SEM; ** p < 0.01 compared to WT miceBack to article page