Research Paper Volume 13, Issue 1 pp 1186—1211

Figure 2. ECFCs isolated from diabetic patients showed dysfunction. (A) Scratch experiments detected the migration ability of ECFCs. (N=3) *P < .05 compared with normal ECFCs. (B) Matrigel assays performed for tube formation experiments identified the angiogenesis of ECFCs. The photos were captured with a 40X microscope. (N=3) *P < .05 compared with normal ECFCs. (C) Single cloned cell proliferation experiments detected the proliferation ability of single cells. Cell number <500 was low clone (LPP), <10,000 was normal clone (MPP), and >10,000 was high clone (HPP). The cell was seeded into a 96-well plate and the ratio of clones was counted. (N=3) *P < .05 versus normal ECFC. (D, E) The proliferative ability of diabetic ECFCs was found to be impaired. The nucleus was dyed blue by Hoechst stain and the proliferating cells were dyed red by 5-ethynyl-2′-deoxyuridine. The photos were captured by a 40X microscope. (N=3) (D). Hemocytometer counting of ECFCs in 24, 48, and 72h after seeding at the density of 2x10⁴cells/well. (N=3) *P < .05 versus normal ECFCs (E). Data shown in the graphs represent mean ± standard deviation.