Fig. 6

Pharmacological ablation of cIAP1 with LCL161 attenuates muscle atrophy. a Primary myoblasts were isolated from C57BL/6 mice and allowed to differentiate for 48 h to produce myotubes. Myotubes were treated with 10 ng/ml TNFα or 50 um dexamethasone (Dex) in the absence or presence of 500 nM LCL161. Untreated (UT) myotubes served as controls. Myotubes were collected for protein 24 h after treatment. Representative Western blots of cIAP1 and GAPDH expression. b Myotubes cultured as in a were stained with MyHC (green) and nuclei were counterstained with DAPI (blue). Representative images are shown. Scale bar = 50 um. Myotube diameter of MyHC+ myotubes in c UT vehicle and LCL161-treated cultures, d TNFα-treated cultures, and e Dex-treated cultures (n = 4). f C57BL/6 mice were treated with vehicle or LCL161 (75 mg/kg) at 4, 7, and 11 days after denervation of the right hind limb. Mice were sacrificed 14 days post-denervation. Representative Western blots of cIAP1 and GAPDH expression in the gas muscle. g Representative images of EDL muscle sections stained with H&E from mice described in f. Scale bar = 20 um. h Loss in TA, Sol, and EDL fiber size as a percentage of non-denervated control leg cross-sectional area (n = 4). Data is the mean ± SEM, *p < 0.05, means with no common letters are significantly different from each other (p < 0.05)