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. 2018 Dec 6;28(8):1244–1259. doi: 10.1093/hmg/ddy405

Figure 4.

Figure 4

siRNA-mediated knock-down of PGC1α is sufficient to cause the hypotrophic FSHD myotube phenotype, which can be rescued by the ERRα agonist biochanin A. (A) RT-qPCR demonstrates that four combined siRNAs against PGC1α successfully suppresses PGC1α (PPARGC1A) in control 54-6 myoblasts. Data expressed as mean ± SEM where an asterisk denotes significant difference (P < 0.05) using an unpaired two-tailed t-test. (B) Control 54-6 myoblasts were transfected with a mixture of four siRNAs against PGC1α or a scrambled siRNA control and induced to differentiate for 3 days. Control 54-6 myoblasts were also transfected with combined siRNAs against PGC1α or a scrambled siRNA control but also exposed to 10 μm biochanin A during 3 days of differentiation. Myotubes were then immunolabelled for MyHC and all nuclei counterstained with DAPI (Magnification: ×100). (C) PGC1α knock-down significantly reduced MyHC+ve area. However, this PGC1α knock-down mediated reduction in MyHC+ve area could be rescued to control levels by administration of 10 μm biochanin A to the differentiation medium. Data expressed as mean ± SEM (n = 3 wells per line) where an asterisk denotes significant difference between the MyHC+ve area in 54-6 control siRNA/untreated versus treated conditions (P < 0.05) using an unpaired two-tailed t-test.