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. 2015 Oct;185(10):2668–2684. doi: 10.1016/j.ajpath.2015.06.008

Figure 9.

Figure 9

Failure to sustain inhibition of muscular dystrophy in Galgt2 transgenic Dag1−/− skeletal muscles. A: Examples of hematoxylin and eosin–stained muscle sections from 2- and 9-month-old wild-type, dystroglycan-deficient (Dag1−/−), and Galgt2 transgenic dystroglycan-deficient (mCTDag1−/−) muscle. B: Quantification of percentage of myofibers with centrally located nuclei in the gastrocnemius (Gastroc), quadriceps (Quad), and tibialis anterior (TA) muscles. C: Quantification of serum creatine kinase activity. D: Semiquantitative real-time PCR measures of relative dystroglycan (Dag1) gene expression at 2 and 9 months, normalized to 1 for 2-month-old wild-type muscle. E: Semiquantitative real-time PCR measures of relative Galgt2 gene expression normalized to 1 for 2-month-old wild-type muscle. Errors are SEM (B and C) or SD (D and E). n = 6 per group (B); n = 4 to 9 per group (C); n = 3 to 6 per group (D and E). ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001. Scale bar = 200 μm (A).