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. 2017 May 25;8:15201. doi: 10.1038/ncomms15201

Figure 4. miR-29b is necessary for muscle atrophy in vitro.

Figure 4

(a) qRT–PCR analysis showed decreased miR-29b, but not miR-29a or miR-29c expressions, in C2C12 myotubes transfected with miR-29b inhibitor compared to negative control (NC inhibitor) (n=6 per group). (b) Immunofluorescent staining for myotubes showed no difference in myotube diameter when C2C12 myotubes were transfected with NC inhibitor and miR-29b inhibitor (n=4 per group, scale bar, 100 μm). (c) miR-29b inhibition abolished Dex (50 μM)-induced muscle atrophy in C2C12 myotubes, as determined by myotube diameter (n=4 per group, scale bar, 100 μm), creatine kinase (CK) activity (n=6 per group) and Atrogin-1 and Murf-1 mRNA levels (n=6 per group). (d) miR-29b inhibition abolished Dex (50 μM)-induced muscle atrophy in myotubes differentiated from primary myoblasts, as determined by myotube diameter (n=4 per group, scale bar, 100 μm), and Atrogin-1 and Murf-1 mRNA levels (n=6 per group). Dex, dexamethasone. Error bars, s.e.m. An unpaired, two-tailed Student's t-test was used for comparisons between two groups (a,b). One-way ANOVA test was performed to compare multiple groups followed by Bonferroni's post hoc test (c,d). *P<0.05, **P<0.01.