Figure 8
From: Annexin A1 Deficiency does not Affect Myofiber Repair but Delays Regeneration of Injured Muscles
Anx A1 deficiency lowers efficiency of fusion for differentiating muscle cells.
(A,B) Muscle sections taken at 7th day post-injury from w.t. (A) and Anx A1−/− (B) mice were labeled with desmin (red) and BrdU (green) antibodies to mark differentiating muscle cells and nuclei of newly divided cells, respectively. Arrowheads mark differentiating but yet unfused myoblasts identified as desmin-and BrdU-positive cells located at the surface of myofibers. Arrows mark nuclei of newly generated myoblasts that had already fused and were identified as BrdU-labeled nuclei in desmin-labeled myofibers. Scale bar 20 μm. (C) The total numbers of fusion-committed myogenic cells in muscle sections taken at 5th and 7th days post-injury were quantified as the sum of the numbers of fused myoblasts (scored as a number of BrdU-labeled nuclei in myofibers) and unfused myoblasts (quantified as desmin- and BrdU- positive cells located within the myofiber basement membrane) normalized to the number of new fibers. (D) The numbers of unfused myoblasts in muscle sections taken 5 or 7 days after injury were normalized to the numbers of new fibers in the same slices. (E) The numbers of unfused differentiating myoblasts in muscle sections taken 7 days after injury were normalized to the total numbers of differentiating myoblasts in the same slices. (C–E) The points show the means for each mouse in a given condition and a line within the group of the points shows the mean of the means for all mice in a given condition. Levels of statistical significance of differences between w.t. and Anx A1-deficient mice are shown as * for p < 0.05; and ** for p ≤ 0.01. The rest of the samples were not significantly different from each other, p > 0.05.
