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Background: The aim of the present study was to investigate whether adipose-derived stem cells could contribute to skeletal muscle-healing. Methods: Adipose-derived stem cells of male rats were cultured and injected into the soleus muscles of female rats. Two and four weeks after injections, muscles were tested fortetanic force (50 Hz). Histological analysis was performed to evaluate muscle collagen deposition and the number of centronucleated muscle fibers. In orderto track donor cells, chimerism was detected with use of real-time polymerase chain reaction targeting the male sex-determining region Y (SRY) gene. Results: Two weeks after cell injection, tetanus strength and the number of centronucleated regenerating myofibers, as well as the number of centronucleated regenerating myofibers, were higher in the treated group than they were in the control group (mean and standard error of the mean, 79.2 ± 5.0% versus 58.3 ± 8.1%, respectively [p < 0.05]; and 145 ± 36 versus 273 ± 18 per 103 myofibers, respectively [p < 0.05]). However, there were no significant differences at four weeks. Treatment did not decrease collagen deposition. Male gene was not detected in female host tissue at two and four weeks after engraftment by polymerase chain reaction analysis. Conclusions: Adipose-derived stem-cell therapy increased muscle repair and force at two weeks, but not four weeks, after injection, suggesting that adipose-derived stem-cell administration may accelerate muscle repair; however, the rapid disappearance of injected cells suggests a paracrine mechanism of action.

The type 2 deiodinase (D2) activates the prohormone T4 to T3. D2 is expressed in skeletal muscle (SKM), and its global inactivation (GLOB-D2KO mice) reportedly leads to skeletal muscle hypothyroidism and impaired differentiation. Here floxed Dio2 mice were crossed with mice expressing Cre-recombinase under the myosin light chain 1f (cre-MLC) to disrupt D2 expression in the late developmental stages of skeletal myocytes (SKM-D2KO). This led to a loss of approximately 50% in D2 activity in neonatal and adult SKM-D2KO skeletal muscle and about 75% in isolated SKM-D2KO myocytes. To test the impact of Dio2 disruption, we measured soleus T3 content and found it to be normal. We also looked at the expression of T3-responsive genes in skeletal muscle, ie, myosin heavy chain I, α-actin, myosin light chain, tropomyosin, and serca 1 and 2, which was preserved in neonatal SKM-D2KO hindlimb muscles, at a time that coincides with a peak of D2 activity in control animals. In adult soleus the baseline level of D2 activity was about 6-fold lower, and in the SKM-D2KO soleus, the expression of only one of five T3-responsive genes was reduced. Despite this, adult SKM-D2KO animals performed indistinguishably from controls on a treadmill test, running for approximately 16 minutes and reached a speed of about 23 m/min; muscle strength was about 0.3 mN/m·g body weight in SKM-D2KO and control ankle muscles. In conclusion, there are multiple sources of D2 in the mouse SKM, and its role is limited in postnatal skeletal muscle fibers.

This work describes the use of ultrasound biomicroscopy (UBM) to follow up the degeneration–regeneration process after a laceration injury induced in the lateral gastrocnemius (LG) and soleus (SOL) muscles of rats. UBM (40 MHz) images were acquired and used for biomechanical characterization of muscular tissue, specifically using pennation angle (PA) and muscle thickness (MT). The animals were distributed in three groups: the variability group (VG; N =5), the gastrocnemius injured group (GG; N =6) and the soleus injured group (SG; N =5). VG rats were used to assess data variability and reliability (coefficients of variation of 9.37 and 3.97% for PA and MT, respectively). GG and SG rats were submitted to the injury protocol in the LG and SOL muscles of the right legs, respectively. UBM images of muscles of both legs were acquired at the following time points: before and after injury (immediately, 7, 14, 21 and 28 days). We observed an increase in PA for the non-injured leg 28 days after injury for both GG and SG rats (GG=10.68 to 16.53 deg and SG=9.65 to 14.06 deg; P