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. 2015 Apr 8;10(4):e0125176. doi: 10.1371/journal.pone.0125176

Fig 3. PGC-1α inhibited hyperglycemia-induced elevation of ROS production as well as mitochondrial fragmentation.

Fig 3

A: Mesangial cells were transfected with PGC-1α short hairpin RNA (shRNA) for 48 h, and PGC-1α protein expression was detected by western blotting. PGC-1α expression was inhibited (~66% reduction) by PGC-1α shRNA. B: PGC-1α expression in transfected mesangial cells. Mesangial cells were transfected with the pcDNA3-PGC-1α (PGC-1α expression) plasmid or empty vector (pcDNA3), with untreated cells used as the control. Expression levels of PGC-1α in the indicated transfectants were analyzed by Western blotting. (C-F) ROS production, mitochondrial morphology changes, and computer-assisted morphometric analyses of mitochondrial morphology in RMCs exposed to normal glucose (NG) and high glucose (HG) conditions, RMCs transfected with PGC-1α shRNA plasmid (NG + PGC-1α shRNA) and shRNA control plasmid (NG+shRNA-con) and exposed to NG conditions, RMCs transfected with pcDNA-PGC-1α plasmid (HG + pcDNA3-PGC-1α) and empty plasmid pcDNA3 (HG + pcDNA3) and exposed to HG conditions, RMCs transfected with PGC-1α shRNA plasmid and DRP1-shRNA plasmid (NG + PGC-1α shRNA+DRP1-shRNA). ***P < 0.001, ** P < 0.01 versus NG, ## P < 0.01, # P < 0.05 versus HG. Scale bar: 10 μm.