-Actinin disorganization in myofibers from tenotomized muscle correlates with scattered MPC proliferation. (A) Representative photomicrographs of X-gal-stained control and tenotomized TA muscles 10 days post-tenotomy. Note the shortening and stronger blue staining of the tenotomized TA muscle compared to the contralateral control muscle, indicating the presence of a large number of Myf5-nLacZ+ MPCs in the tenotomized TA muscle. (B) Representative images of X-gal-stained longitudinal sections from the same regions of TA muscles from Myf5-nlacZ mice. The number of MPCs was quantified by counting the number of lacZ-expressing MPCs in the tenotomized TA and contralateral control muscles (three sections per muscle). (C) Histograms showing the total number of quiescent and proliferating MPCs (Myf5+ cells). These results were obtained by counting the number of Myf5+ cells per field in the same regions of the tenotomized TA and contralateral muscles (three sections per muscle) (n = 5 mice). (D) Representative photomicrographs of a tenotomized TA muscle showing α-actinin (green) disorganization (top panels) and MyoD+ cells (green) (bottom panels). (E) Box-and-whisker plot (90th percentile) showing the average width (left panel) and periodicity (right panel) of myofibers in tenotomized TA muscles compared to intact contralateral control muscles (n = 38 for intact TA muscles and n = 66 for tenotomized TA muscles; n = 4 mice). An F-test for equality of variances was used to determine the distribution of measurements in the two groups (intact versus tenotomized muscles) (F) Representative photomicrographs of MyoD immunostaining showing a large number of MyoD+ cells scattered among the disorganized myofibers of tenotomized muscles. *P < 0.05, **P < 0.01, ***P < 0.0001, and ****P < 0.00001 versus the contralateral control muscle. All results are expressed as means ± SEM.