Fig. 5

The neovascularization and wound healing were improved by neutralization of CXCL5 antibodies in type 2 DM mice. Treatment with CXCL5 mAb reduced CXCL5 levels in diabetic mice (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 db/db mice (n = 6; B). The number of circulating EPCs was determined by flow cytometry in db/db mice. Treatment with CXCL5 mAb 100 μg increased the number of circulating EPCs after ischemia surgery compared with DM (n = 6; C). Anti-CD31 immunostaining showed that CXCL5 mAb 100 μg treatment 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 images and analysis of hemoglobin content (n = 6; F). Representative matrigel plug images with immunostaining of CD31. CD31 positive areas were enhanced in the CXCL5 mAb 100 μg treatment mice. Scale bar, 50 µm (G). CXCL5 mAb 100 μg treatment improved wound repair ability in db/db 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 mAb 100 μg treatment mice. Scale bar, 50 µm (I). Serum concentration of VEGF and SDF-1 were higher in the CXCL5 mAb 100 μg treatment mice (n = 6; J, K). CXCL5 Chemokine C-X-C motif ligand 5, DM diabetes mellitus, EPC endothelial progenitor cell, mAb monoclonal antibody, SDF-1 stromal cell-derived factor 1, VEGF vascular endothelial growth factor. The Mann–Whitney U test was used to determine statistically significant differences. *p < 0.05, **p < 0.01 compared with the non-DM control. ^#p < 0.05, ^##p < 0.01 compared with the untreated DM group