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. 2014 Dec 15;211(13):2617–2633. doi: 10.1084/jem.20140317

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© 2014 Di Foggia et al.

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Figure 1. — Bmi1 expression in mouse models of acute and chronic skeletal muscle injuries. (a) Schematic representation of satellite cell isolation after freeze injury in C57BL/6J mice. (b) Relative Bmi1 expression represented as 1/dCT values at 3 d.a.i. and 10 d.a.i. (mean ± SEM from three independent experiments with n = 3 uninjured, n = 3 3 d.a.i., and n = 2 10 d.a.i.; ***, P < 0.001). (c) Immunofluorescence for Pax7 and Bmi1 on muscle sections from uninjured mice, injured mice (10 d.a.i.), and mdx mice (representative results from n = 4 uninjured, n = 2 3 d.a.i., n = 2 10 d.a.i., and n = 4 mdx). Arrows indicate Bmi1 staining intensity (expression level) in Pax7^+ve satellite cells in three different conditions (uninjured, 10 d.a.i., and mdx). (d) Quantification of Bmi1 staining of Pax7^+ve cells with pixel intensity above 400 at 3 and 10 d.a.i. compared with uninjured controls (mean ± SEM from two independent experiments with n = 4 uninjured, n = 2 3 d.a.i., n = 2 10 d.a.i., and n = 4 mdx; *, P < 0.05). (e) Bmi1 expression in satellite cells obtained from mdx single fibers after switching from growth to differentiation-inducing culturing conditions (48 h in differentiation conditions) compared with control satellite cells (mean ± SEM from two independent experiments with n = 3 for each condition; *, P < 0.05). Bar, 50 µm.