Aim To evaluate the ability of capillary network formation of HUCB-late EPCs in vitro and in rat hind limb ischemic tissues, after transfected with rAAV-CXCR4 and rAAV-GFP. Methods HUCB-late EPCs were infected with rAAV₆-CXCR4、rAAV₆-GFP, and the expression of CXCR4 protein was detected by Western Blot analysis. In vitro,evaluate the ability of capillary network formation on Matrigel between the three groups. The mode of mouse hind limb ischemia was set up, by ligating the femoral artery and its branches. Following successful establishment,18 rats were divided into three groups randomly:blank group were intramuscularly injected with 500 μL EGM-2 at 6 hours following injury,and control group were intramuscularly injected with 500 μL EGM-2 at 6 hours following injury (contain 1×10⁶ non-gene transfected HUCB-late EPCs), and experiment group were intramuscularly injected with 500 μL EGM-2 at 6 hours following injury (contain 1×10⁶ CXCR4-gene transfected HUCB-late EPCs). After 28 days, capillary network in hind limb muscles and next to muscles were detected by HE stain assay,and CD31 expressed in neovascularization endothelial cells were detected by immune histochemistry assay,and calculate the number of CD31 positive neovascularization, and calculate the number of CD31 positive neovascularization. ResultsCompared with infected rAAV6-GFP and non-infected group, the expression of CXCR4 protein was up-regulated after infected rAAV₆-CXCR4. In vitro, there is no significance of tube area in unit area among three types of HUCB-late EPCs (P>0.05). In the mode of mouse hind limb ischemia, compared with blank group and control group, CD31 positive cells of new capillary network in experimental group increased obviously(P<0.05). Conclusion CXCR4 over-expression of HUCB- late EPCs could promote neovascularization in rat hind limb ischemic tissues.