Intercellular mitochondrial transfer as a means of revitalizing injured glomerular endothelial cells

Figure 2 Mesenchymal stem cells alleviate mitochondrial activity and high glucose-induced oxidative stress in cultured glomerular endothelial cells. A: Mesenchymal stem cells (MSCs) increased adenosine triphosphate production in high glucose (HG)-induced glomerular endothelial cells (GECs); B: MSCs also attenuated mitochondrial membrane potential (ΔΨm) in GECs. Carbonyl cyanide 3-chlorophenylhydrazone as a mitochondrial oxidative phosphorylation uncoupler, was used as the positive control group; C: Effect on mitochondrial fission marker and the fusion marker levels; D: Pretreatment with MSCs attenuated HG-induced upregulation in DCF-DA [intracellular reactive oxygen species (ROS)] and MitoSOX Red (mitochondrial ROS) fluorescent intensity; E: Representative western blot expression levels of ROS-protective enzymes (superoxide dismutase 2 and glutathione peroxidase 3); F: Concentration of interleukin (IL)-6 in the supernatant by enzyme-linked immunosorbent assay; G: Mitochondrial transfer ameliorated the mRNA expression levels of inflammatory markers (tumor necrosis factor-α and IL-1β), as determined using real-time reverse transcriptase-polymerase chain reaction. Data are presented as the mean ± SD. ^aP < 0.05 vs normal control group, ^bP < 0.01 vs normal control group, ^cP < 0.05 vs high glucose group. MSCs: Mesenchymal stem cells; DRP1: Dynamin-related protein 1; MFN2: Mitofusin 2; ROS: Reactive oxygen species; SOD2: Superoxide dismutase 2; GPx-3: Glutathione peroxidase 3; IL-6: Interleukin-6; CCCP: Carbonyl cyanide 3-chlorophenylhydrazone; NC: Normal control; HG: High glucose; TNF-α: Tumor necrosis factor-α; ATP: Adenosine triphosphate.