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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Neurobiol Dis. 2016 Mar 19;91:247–261. doi: 10.1016/j.nbd.2016.03.015

Figure 5. Effects of Mic60 Knockdown on mitochondrial respiration in differentiated SH-SY5Y cells.

Figure 5

Differentiated SH-SY5Y cells were transfected with empty vector EV-shRNA, negative control GFP-shRNA, or Mic60 shRNA shRNA’08. On day 3 after transfection, cells were treated with either DMSO vehicle (A,B,E) or 0.1 μM rotenone (C,D,F) for 24 hr, then assessed for mitochondrial function via a mitochondrial stress test using a Seahorse XF96 extracellular flux respirometer. (A,C) Oxygen consumption rate (OCR) was normalized to post-analysis immunocytochemical quantification of MAP2 protein levels, and is expressed as (pmol oxygen consumption/min)/MAP2 level. (B,D) The three measurements per stress group (Oligomycin, FCCP, and Rotenone & AntimycinA) were averaged per n for one value of respiration, and then averaged across all experiments. (E–F) Reserve capacity of respiration was calculated for each n from the difference between average basal and average maximal respiration, and then averaged across all experiments. (n=18 for DMSO control, n=12 for 0.1 μM rotenone, from 3 independent experiments; mean ± SEM; * = Mic60-shRNA significant from EV-shRNA and GFP-shRNA, p<0.05)