Androgen-dependent pathology demonstrates myopathic contribution to the Kennedy disease phenotype in a mouse knock-in model
J. Clin. Invest. Zhigang Yu, et al. 116:2663 doi:10.1172/JCI28773 [Go to this article.]

Figure 5
Levator ani/bulbocavernosus muscles exhibit severe pathology in young AR113Q males. (A) Representative images of levator ani/bulbocavernosus muscle from WT and AR113Q males. Magnification, ×400 (top row). Frequent AR immunoreactive intranuclear inclusions were present in muscle from AR113Q but not WT mice. Magnification, ×1000 (middle row). Muscle from castrated AR113Q males also contained frequent AR immunoreactive intranuclear inclusions. Magnification, ×1000 (bottom row). (B) Altered expression of myogenin and acetylcholine receptor α-subunit mRNA but not MyoD mRNA in AR113Q muscle. Relative mRNA expression levels were determined by quantitative real-time RT-PCR. Data are from WT (n = 7), AR113Q (n = 8), and castrated WT males (n = 6) at 3–5 months and surgically castrated AR113Q males at 18 months (n = 4). Results are reported as mean ± SD relative to expression of 18s rRNA. Differences between WT and AR113Q are significant at P < 0.05 for myogenin and acetylcholine receptor α-subunit mRNA by ANOVA with the Neuman-Keuls multiple comparison test. Expression of MyoD mRNA is not different between WT and AR113Q.