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. 2017 Apr 1;31(7):648–659. doi: 10.1101/gad.293266.116

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© 2017 Latella et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 1. — MuSCs isolated from mdx/mTR mice display impaired differentiation, up-regulation of senescence markers, and DNA damage accumulation through disease progression. (A) Schematic representation of a MuSC differentiation experiment. (B) Immunofluorescence for MyHC (green) and DAPI (4′,6′-diamino-2-phenylindole) (blue) in MuSCs isolated from 9.5- to 11-mo-old mice and induced to differentiate for 3 d. (C) Differentiation index. (D) Quantitative PCR (qPCR) on isolated MuSCs from mdx/TR wild-type (WT), heterozygous (Het), G1, and G2 mice normalized for GAPDH. (E) Immunofluorescence for PAX7 (green), γH2AX (red), Laminin (white), and DAPI (blue) in gastrocnemius muscles isolated from 2-mo-old (young) and 18- to 24-mo-old (old) mdx/mTR mice. (F) Quantification of PAX7- and γH2AX-coexpressing cells. Bar, 25 µm.