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. 2017 Jun 12;36(14):2126–2145. doi: 10.15252/embj.201696179

Figure 7. OPA1 deletion in primary myotubes confirms a role for OPA1‐induced mitochondrial dysfunction and ER stress on FGF21 secretion.

Figure 7

  1. Representative immunoblots in primary myotubes obtained from OPA1fl/fl mice and infected with Ad‐GFP or Ad‐Cre. Cells were treated with either vehicle (PBS) or PBA for 3 days. Densitometric analysis of immunoblots of OPA1, CHOP, XBP‐1, and FGF21 normalized to GAPDH protein levels and of pAMPK/AMPK ratios (n = 6).
  2. Secreted FGF21 levels measured in the media (n = 6).
  3. Measurement of oxygen consumption rates (OCR) in primary myotubes 3 days after adenoviral infection (n = 8–10 technical replicates).
  4. Measurements of extracellular acidification rates during a glycolysis stress test in primary myotubes 3 days after adenoviral infection (n = 8–10 technical replicates).
  5. TMRM fluorescence over time after treatment with H2O2 (n = 3 technical replicates).
  6. Representative pictures of primary myotubes stained with TMRM at times 0 (immediately after addition of H2O2) and 100 min after H2O2 treatment. Scale bar = 100 μm.
Data information: Data are expressed as means ± SEM. Significant differences were determined by Student's t‐test (C–E), using a significance level of P < 0.05; (*) significantly different vs. WT cells or by ANOVA followed by Tukey multiple comparison test (A, B), using a significance level of P < 0.05 for the studies in which cells were treated with PBA. (*) vs. WT; (#) vs. KO. Source data are available online for this figure.