Figure 3.

Inducible deletion of Rbm24 delays skeletal muscle regeneration. (A) Schematic representation of CTX-induced injury and tamoxifen administration. The TA muscle was harvested at the indicated time points following injury. (B) Validation of Rbm24 knockout in the injured TA muscle at 5 D.P.I using western blotting. GAPDH was used as a loading control. (C) Gross morphology analysis of regenerated TA muscle at 28 D.P.I. The smaller regenerated muscle mass in UKO mice showed the delayed regeneration process. Scale bars, 2 mm. (D) Statistical analysis of regenerated TA muscle mass (n = 7 per group). (E) H&E staining showing deficient regeneration in the UKO mice. The increased myofibers with smaller sizes in the UKO mice were indicated by the arrowheads. Scale bars, 50 µm. (F) Statistical analysis of the average CSA of regenerated myofibers with centrally located nuclei. The CSA of the regenerated myofibers was significantly decreased in the UKO mice. At least 1,200 myofibers were analyzed in each mouse (n = 7 per group). (G) Distribution of regenerated myofibers with different CSA. There was a striking left shift in the UKO mice compared with the WT mice. At least 1,200 myofibers were analyzed in each mouse (n = 7 per group). Data are presented as the mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001; unpaired t-test. Abbreviations: CSA: cross-sectional area; CTX: cardiotoxin; D.P.I: days post injury; NS: not significant; TA muscle: tibialis anterior muscle; UKO: UBC-CreERT2, Rbm24^loxP/loxP; WT: wild type.