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. Disclosure: One or more of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of an aspect of this work. None of the authors, or their institution(s), have had any financial relationship, in the thirty-six months prior to submission of this work, with any entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. Also, no author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article.

This study tests the hypothesis that bone marrow-derived mononuclear cell (BMDMC) therapy may reduce lung inflammation and fibrosis leading to an improvement in respiratory mechanics in a murine model of silicosis.52 female C57BL/6 mice were randomly assigned into four groups. In the silica group (SIL), silica suspension (20 mg/50 mL in saline) was intratracheally instilled. In the control animals, 50 mL saline was administered intratracheally. At 1 h, the control and SIL groups were further randomised, receiving BMDMC (2610 6 In the SIL-cell group, the fraction area of granuloma, the number of macrophages and the collagen fibre content were reduced, yielding improved lung mechanics. The presence of male donor cells in lung tissue was not confirmed using detection of Y chromosome DNA. Nevertheless, caspase-3, IL-1b, IL-1a, IL-1RN and TGF-b mRNA expression diminished after cell therapy.In conclusion, BMDMC acted on inflammatory and fibrogenic processes improving lung function through paracrine effects.

The hypothalamic-pituitary-thyroid axis is affected by acute exercise, but the mechanisms underlying thyroid function changes after exercise remain to be defined. The aim of this study was to elucidate the effects of a session of acute exercise on the treadmill at 75% of maximum oxygen consumption on thyroid function of rats. Male Wistar rats were divided into five groups: control (without exercise), and killed immediately after (0 min) or 30, 60, and 120 min after the end of the exercise session. A significant increase in serum tri-iodothyronine (T 3 ) occurred immediately after the exercise, with a gradual decrease thereafter, so that 120 min after the end of the exercise, serum T 3 was significantly lower than that in controls. Total thyroxine (T 4 ) increased progressively reaching values significantly higher than that in the control group at 120 min. T 3 /T 4 ratio was significantly decreased 60 and 120 min after the exercise, indicating impaired T 4 -to-T 3 conversion. Liver type 1 deiodinase activity (D1) significantly decreased at 60 and 120 min, while pituitary D1 increased progressively from 30 to 120 min after the exercise, and thyroid D1 was increased only immediately after the end of the exercise. Brown adipose tissue (BAT) type 2 deiodinase activity (D2) was significantly lower at 30 min, but pituitary D2 remained unchanged. No change in serum thyrotropin was detected, while serum corticosterone was significantly higher 30 min after the exercise. Our results demonstrate that decreased liver D1 and BAT D2 might be involved in the decreased T 4 -to-T 3 conversion detected after an exercise session on the treadmill.

These data clearly shows that G-CSF treatment was unable to prevent cardiac remodeling or to improve cardiovascular function in a rat model of acute myocardial infarction, by permanent LAD ligation, despite bone marrow stem cell mobilization.

Skeletal muscle injury is the most common problem in orthopedic and sports medicine, and severe injury leads to fibrosis and muscle dysfunction. Conventional treatment for successive muscle injury is currently controversial, although new therapies, like cell therapy, seem to be promise. We developed a model of successive injuries in rat to evaluate the therapeutic potential of bone marrow mesenchymal cells (BMMC) injected directly into the injured muscle. Functional and histological assays were performed 14 and 28 days after the injury protocol by isometric tension recording and picrosirius/Hematoxilin & Eosin staining, respectively. We also evaluated the presence and the fate of BMMC on treated muscles; and muscle fiber regeneration. BMMC treatment increased maximal skeletal muscle contraction 14 and 28 days after muscle injury compared to non-treated group (4.5 ± 1.7 vs 2.5 ± 0.98 N/cm2, p<0.05 and 8.4 ± 2.3 vs. 5.7 ± 1.3 N/cm2, p<0.05 respectively). Furthermore, BMMC treatment increased muscle fiber cross-sectional area and the presence of mature muscle fiber 28 days after muscle injury. However, there was no difference in collagen deposition between groups. Immunoassays for cytoskeleton markers of skeletal and smooth muscle cells revealed an apparent integration of the BMMC within the muscle. These data suggest that BMMC transplantation accelerates and improves muscle function recovery in our extensive muscle re-injury model.