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Fig. 2. Lack of Mstn facilitates muscle regeneration. Tibialis anterior muscle from wild-type and Mstn^-/- mice were injured using notexin, and frozen muscle samples were sectioned. (A) Hematoxylin and eosin staining of control uninjured muscle sections from wild-type and Mstn^-/- mice are shown. (B) One day (D1) after the notexin treatment there was extensive muscle necrosis in both wild-type and Mstn^-/- mice (low power view shown in B). (C) Myofibers contained eosinophilic (e) cytoplasm and some cells showed fine intracellular vacuolation (v). There was an increase in the intracellular spaces with marked myofiber disruption visible (arrows). (D) In day 2 Mstn^-/- muscle sections (D2), increased numbers of nuclei within the injured area were seen (arrows). Arrow heads denote the myonuclei along the margins of the necrotic myofibers. (E) Three days after notexin treatment (D3), both muscle sections have infiltrating mononucleated cells, but higher numbers were present in the Mstn^-/- sections. (F) In day 5 sections (D5), increased numbers of nuclei were seen within the injured area of Mstn^-/- muscle sections. (A,C-F) Bar, 10 µm. (B) Bar, 100 µm.

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