A role for Regulator of G protein Signaling-12 (RGS12) in the balance between myoblast proliferation and differentiation
Fig 8
Rgs12 mRNA is upregulated in skeletal muscles of Dmdmdx mice, but RGS12 loss does not appear to alter the muscle wasting phenotype of the Dmdmdx mouse model.
A, Representative micrographs of quadriceps femoris muscle from indicated mice, labeled with wheat-germ agglutinin (WGA; green) and nuclear DNA (blue). Loss of RGS12 in satellite cells does not alter skeletal muscle morphology of mdx mice. B, Rgs12 expression was elevated in the diaphragm (*, p<0.05) and quadriceps femoris (***, p<0.001) muscles of mdx mice as assessed by qRT-PCR analysis. Bar graph displays the mean ± SEM; differences between wild-type and mdx mice were shown to be statistically significant by Student’s t-test. C, The maximal tetanic isometric plantar flexor tension normalized to body weight of Rgs12fl/fl; Pax7::Cre mice (n = 5), wild-type Pax7::Cre mice (n = 5), Rgs12fl/fl; Pax7::Cre; mdx mice (n = 5), and wild-type Pax7::Cre; mdx mice (n = 5) obtained at 6, 12, and 24 weeks of age are displayed as mean ± SEM. A two-way ANOVA indicated mdx mice had impaired muscle function relative to Dmd wild-type mice at each age; however, Rgs12 deficiency did not alter muscle function in mdx or Dmd wild-type mice.