Fig. 7. Overexpression of SELENOW alleviates myotube atrophy in vitro.

(A) Immunofluorescent staining of MyHC in C2C12 myotubes. Before DEX treatment, the myotubes were infected with a control vehicle or a SELENOW vehicle; scale bars, 100 μm. (B) Quantification of these C2C12 myotube; at least 150 myotubes in one group were measured. (C) Expression of SELENOW in mRNA level of C2C12 myotube, n = 4. (D and E) Western blot analysis for the protein levels of MyHC, Atroging-1, and MuRF-1 in these C2C12 myotubes; β-actin was used as the loading control, n = 4. (F) Immunofluorescent staining of MyHC in primary myotubes. Before DEX treatment, the primary myotubes were infected with a control vehicle, a SELENOW vehicle, or a SELENOW (Ser¹³) vehicle; scale bars, 100 μm. (G) Quantification of these primary myotube diameters; at least 500 myotubes in one group were measured. (H) Expression of MyHC, Atrogin-1, MuRF-1, and SELENOW in the mRNA level of these primary myotubes; GAPDH was used as the loading control, n = 5 to 6. Data are means ± SEM; labeled means without a common letter differ; P < 0.05.