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. 2013 Jul 12;169(7):1461–1476. doi: 10.1111/bph.12197

Figure 2.

Figure 2

The induction of mitochondrial biogenesis by EH-201 is mediated by EPO. (A, B) EH–201-treated kidney slices and primary cardiomyocytes and (C, D) EH–201-treated hepatocytes and C2C12 myotubes with or without the neutralizing EPO antibody (nEPO-ab, 1 μg·mL−1) were analysed for PGC-1α expression by QPCR (n = 6) and Western blotting (n = 4), citrate synthase activity (n = 3), and mtDNA copy number (n = 6) and via the MitoTracker assay (n = 6). The control represents vehicle treatment. (E, F and G) rhEPO was given to kidney slices, hepatocytes and C2C12 myotubes. The mitochondrial activity was determined by PGC-1α Q-PCR (n = 6), citrate synthase activity (n = 3), mtDNA copy number (n = 6), and MitoTracker assays (n = 6). The control represents vehicle treatment. PGC-1α siRNA-transfected C2C12 myotubes were treated with rhEPO (n = 6). The control represents the scrambled siRNA treatment. The values are presented as the means ± SEM. **P < 0.01, *P < 0.05 versus untreated control, n.s., not significant, Student's t-test.