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. 2012 Jul 27;446(Pt 1):23–36. doi: 10.1042/BJ20112024

Figure 7. C26 CM promoted ROS induction, mitophagy and increased autophagy–lysosome pathway activity.

Figure 7

(A) Representative micrographs demonstrating ROS induction in myoblasts treated with CM for 1 or 2 h. Scale bars represent 100 μm. (B) Histogram represents the relative green fluorescence intensity in arbitrary units (A.U) calculated using ImageJ software. Values are means±S.D. (C) An OxyBlot assay demonstrating the amounts of oxidized proteins in myotubes after treatment with (+) or without (−) CM. (D) Histogram represents the qPCR quantification of the mtDNA/nuDNA ratio in control or CM-treated myoblasts. n=4; values are means±S.D. (E) Histogram represents the qPCR quantification of the mtDNA/nuDNA ratio in TA muscle isolated from day 17 C26 tumour-bearing mice (C26 tumour) and control mice. n=5; values are means±S.D. (F) Immunoblot analysis of LC3-I into LC3-II conversion in control (−) and CM-treated (+) C2C12 myotubes incubated for 24 and 36 h. (G) Immunoblot analysis of LC3-I into LC3-II conversion in C2C12 myotubes treated with CM and CM+sActRIIB for 24 h. (H) Immunoblot analysis of LC3-I into LC3-II conversion in TA muscle isolated from control CD2F1 mice (−) and 17 day C26 tumour-bearing CD2F1 mice (+). Statistical significance was assessed by Student's t test compared with the control; *P<0.01. Ctrl, control; IB, immunoblot.