Fig. 6

The neovascularization and wound healing were improved in STZ-induced CXCL5KO diabetic mice. CXCL5 knockout mice had rarely circulating CXCL5 (n = 6; A). Representative evaluation of the ischemic (right) and nonischemic (left) hindlimbs before, immediately after 2 weeks and 4 weeks after the hindlimb ischemia surgery in STZ induced type 1 diabetic mice (n = 6; B). The number of circulating EPCs was determined by flow cytometry in STZ induced type 1 diabetic mice. Deletion of CXCL5 expression increased the number of circulating EPCs after ischemia surgery compared with DM (n = 6; C). Anti-CD31 immunostaining showed that inhibition of CXCL5 expression significantly increased the number of capillaries. Scale bar, 50 µm (n = 6; D). Western blotting and statistical analyses of VEGF and SDF-1 in the ischemia leg (n = 3; E). Representative matrigel plug and analysis of hemoglobin content (n = 6; F). Representative matrigel plug images with immunostaining of CD31. CD31 positive areas were enhanced in the CXCL5 knockout diabetic mice. Scale bar, 50 µm (G). CXCL5 inhibition by knockout improved wound repair ability in STZ induced type 1 diabetic mice. Representative wound areas and the closure rates of 3-mm punch biopsies were measured (n = 6; H). Representative wound area images with immunostaining of CD31. CD31 positive areas were enhanced in the CXCL5 knockout mice. Scale bar, 50 µm (I). CXCL5, Chemokine C-X-C motif ligand 5; CXCL5KO, CXCL5-knockout mice; CXCL5KO+STZ, CXCL5 knockout diabetic mice. DM diabetes mellitus, EPC endothelial progenitor cell, STZ streptozotocin, WT wild-type mice, WT+STZ wild-type diabetic mice. The Mann–Whitney U test was used to determine statistically significant differences. *p < 0.05, **p < 0.01 compared with the WT group. ^#p < 0.05, ^##p < 0.01 compared with the WT+STZ group