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. 2015 Jun 25;5:11594. doi: 10.1038/srep11594

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Copyright © 2015, Macmillan Publishers Limited

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(a) Mononuclear cells isolated from non-diabetic people, as a negative control. (b) Mononuclear cells isolated from non-diabetic people were labeled with PE-CD34 and APC-VEGFR2/KDR (Flk-1) antibodies. Double-positive cells were isolated by sorting on a FACSAria II SORP. (c) Mononuclear cell isolated from diabetic patients were labeled with PE-CD34 and APC-VEGFR2/KDR (Flk-1) antibodies. (d) TEM confirmed the presence of autophagosomes in the EPCs; arrows were used to show the autophagosomes. (e) Quantitative analysis of the number of autophagosomes in the control and diabetes groups (n = 10, *p < 0.05). (f) The inhibition of EPC LC3-I to LC3-II conversion and the increase of EPC mTORC1 in diabetes. We used cropped gels; the gels were run using the same experimental conditions. (g,h) The expression of LC3-I, LC3-II and mTORC1 in the control and diabetes groups. β-actin was used as a loading control (n = 10, *p < 0.05). (i,j) The mean fluorescence intensity of rhodamine 123 in the control and diabetes groups. The mitochondrial membrane potential of EPCs in the diabetic patients was higher than that in the healthy people (n=10, *p < 0.05). (k,l) The mean fluorescence intensity of MDC in the control and diabetes groups. The level of autophagy in the diabetic patients was much lower than that in the healthy people (For Fig. 1i and k, red = non-diabetic control subjects; blue= diabetic patients) (n = 10, *p < 0.05).