Fig. 4.

Diabetes induces mitochondrial fragmentation of EPCs and impairs mitochondrial function. (A) Micrographs of mitochondrial morphology of EPCs were visualized by MitoTracker Red CMXRos probe staining, and the morphological alterations were quantified by Image J and expressed as mitochondrial interconnectivity. (B–C) The expression of mitochondrial fusion and fission related proteins was determined by Western blot, the quantitative data was normalized by the average of Healthy-EPC for each protein, and β-actin was used as a loading control. The levels of (D) intracellular ROS, (E) mitochondrial ROS, and (F) mitochondrial membrane potential were detected by DHE, MitoSOX™, and TMRM staining, respectively, and quantified by a flow cytometry and normalized by the average fluorescence density of Healthy-EPCs. (G) ATP concentration in EPCs was measured by an ATP assay Kit. n = 8 per group. Data shown in graphs represents the means ± SD. *p < 0.05, vs Healthy-EPC. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)