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Fig. 3. Lack of Mstn increases the accretion of myoblasts and macrophages. In a unit regenerating area (20 mm2), Myod1+ or Mac-1+ nuclei were counted and expressed as percentage of the total nuclei identified by DAPI incorporation. The results were an average of three independent sections and the counting of the nuclei was carried out in triplicate on individual sections. (A) Twice the number of Myod1+ myogenic precursor cells were present in the regenerating area of Mstn-/- sections at all times as compared with wild type, indicating a greater migration and/or increased proliferation of myoblasts in the regenerating muscle. (B) Anti-Myod1 immunostaining of regenerating muscle (day 2) from wild-type and myostatin-null (Mstn-null) mice. A DAPI-counterstained section is displayed within the inserts. Examples of positive nuclei and cells are indicated with an asterisk (*). Bar, 10 µm. (C) Anti-Mac-1 antibodies were used to identify infiltrating macrophages. An enhanced inflammatory response in the Mstn-/- muscle is observed at day 2 compared with the wild-type muscle. The number of macrophages in the wild-type muscle was maximum on day 3 and macrophages were still present on day 5 in the wild-type muscle. However, macrophages were not detectable on day 5 in the Mstn-/- muscle section. (**P>0.001; *P>0.01). (D) Anti-Mac-1 immunostaining of regenerating muscle (day 2) from wild-type and myostatin-null (Mstn-null) mice. A DAPI-counterstained section is displayed within the inserts. Examples of positive nuclei and cells are indicated with an asterisk (*). Bar, 10 µm. (E) Expression profiles of genes in control uninjured muscle and regenerating wild-type and Mstn-/- muscle are shown. Quantitative RT-PCR was performed for Myod1 and Myog. The amplicons were detected by Southern blot hybridization. GAPDH was used to show equal amount of RNA used.
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