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. 2018 Nov 19;9:4849. doi: 10.1038/s41467-018-07057-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Tamoxifen treatment improves Mtm1 knockout mouse muscle structure. a Tibialis anterior muscle stained with hematoxylin and eosin (H&E) and succinate dehydrogenase (SDH), and by anti-dysferlin immunofluorescence (IF). Untreated Mtm1 KO muscle has centrally located nuclei (arrows in H&E), mitochondrial aggregation on SDH staining, and abnormal distribution of dysferlin staining. High-dose TAM treatment in KOs results in: (1) reduction of central nuclei (arrowheads); (2) improvement in myofiber size; (3) resolution of mitochondrial aggregation; and (4) restoration of dysferlin to the sarcolemmal membrane. Low-dose TAM improves dysferlin localization but does not resolve central nucleation and myofiber hypotrophy. All drug treatments started at 21 days, and histopathology performed at 36 days of age. b High-dose TAM treatment increases myofiber size of Mtm1 KOs. TAM treated WT (29 ± 3 μm, n = 4) vs. untreated Mtm1 KO (19 ± 3 μm, n = 4, ****p < 0.0001 vs. WT), vs. TAM treated KO (28 ± 3 μm, n = 6, **p = 0.0065 vs. untreated KO, not significant vs. WT + TAM). c High-dose TAM treatment reduces % central nuclei in Mtm1 KOs (per 100 fibers): TAM treated WT (0%, n = 4) vs. untreated Mtm1 KOs (3 ± 0.8%, n = 4, ***p = 0.0004 vs. WT), vs. TAM treated KOs (1.1 ± 0.09%, n = 5, **p = 0.0024 vs. KOs and n.s. vs. WT + TAM). d High and low-dose TAM treatment restores dysferlin localization to cell membrane. Untreated Mtm1 KO = 60 ± 13% cytoplasmic (n = 3, ***p = 0.0002 vs. WT), KO + high TAM = 9 ± 1% cytoplasmic (n = 3, ***p = 0.0005 vs. KO, ns compared to WT + TAM). For low-dose TAM, Mtm1 KO = 66 ± 11% cytoplasmic, (n = 3, ****p = < 0.0001 vs. WT) vs. KO + low TAM = 12 ± 4% cytoplasmic (n = 4, ****p < 0.0001 vs. KO, ns compared to WT + TAM). All data points for b–d presented in Supplementary Table 2. Statistical analyses were conducted by two-way ANOVA, followed by Tukey’s multiple comparisons post-test or Fisher’s Least Common Differences post-test. For direct two sample comparison, unpaired, parametric two-tailed Student's t-test was performed. Scale bars = 20 µm