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Muscle Repair (muscle + repair)
Selected AbstractsEffect of anti-inflammatory and antioxidant drugs on the long-term repair of severely injured mouse skeletal muscleEXPERIMENTAL PHYSIOLOGY, Issue 4 2005A. Vignaud Non-steroidal anti-inflammatory drugs are frequently prescribed after skeletal muscle injury. It is not known whether this type of medication can interfere with muscle repair, although inflammatory response is thought to play an important role in this process. Tibialis anterior muscles of mice were injured by myotoxic agent (snake venom) or crushed. Then, animals were treated daily for 10,14 days with different types of non-steroidal anti-inflammatory and antioxidant drugs. The long-term repair was studied 10,42 days after injury by analysing the recovery of in situ muscle force production, size of regenerating muscle cells and expression of myosin heavy chain. Our results show that diclofenac, diferuloylmethane (curcumin), dimethylthiourea or pyrrolidine dithiocarbamate treatment did not significantly affect muscle recovery after myotoxic injury (P > 0.05). Similarly, diferuloylmethane, dimethyl sulphoxide or indomethacin administration did not markedly change muscle repair after crush injury. However, we noted that high doses (> 2 mg kg,1) of diferuloylmethane or indomethacin increased lethality and reduced muscle repair after crush injury. In conclusion, non-steroidal anti-inflammatory and antioxidant drugs did not exhibit long-term detrimental effects on muscle recovery after injury, except at lethal doses. [source] Skeletal Myoblast Transplant in Heart FailureJOURNAL OF CARDIAC SURGERY, Issue 4 2003Eugene K.W. Sim F.R.C.S. Heart transplantation has emerged as a viable option but is fraught with problems of supply. Mechanical assist devices are extremely expensive and dynamic cardiomyoplasty has shown only limited success in the clinical setting. Recent insights into the pathogenesis of myocardial diseases and the progress made in the field of molecular biology have resulted in the development of new strategies at molecular as well as cellular levels for cardiac muscle repair. One such strategy is to augment ventricular function by means of cellular cardiomyoplasty through intracardiac cell grafting using adult and fetal cardiomyocytes, stem cells, and autologous skeletal myoblasts. (J Card Surg 2003; 18:319-327) [source] Novel glycosaminoglycan mimetic (RGTA, RGD120) contributes to enhance skeletal muscle satellite cell fusion by increasing intracellular Ca2+ and calpain activityJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2005M. Zimowska Glycosaminoglycans (GAG) are classes of molecules that play an important role in cellular processes. The use of GAG mimetics called regenerating agent (RGTA) represents a tool to investigate the effect of GAG moiety on cellular behavior. A first member of the RGTA family (RG1192), a dextran polymers with defined amounts of sulfate, carboxymethyl, as well as hydrophobic groups (benzylamide), was shown to stimulate skeletal muscle repair after damage and myoblast differentiation. To obtain a comprehensive insight into the mechanism of action of GAG mimetics, we investigated the effect on myoblast differentiation of a novel RGTA, named RGD120, which was devoid of hydrophobic substitution and had ionic charge similar to heparin. Myoblasts isolated from adult rat skeletal muscles and grown in primary cultures were used in this study. We found that chronic treatment with RGD120 increased the growth of adult myoblasts and induced their precocious fusion into myotubes in vitro. It also partially overcame the inhibitory effect of the calpain inhibitor N -acetyl-leu-leu-norleucinal (ALLN) on these events. Western blot and zymography analyses revealed that milli calpain was slightly increased by RGD120 chronic treatment. In addition, using fluorescent probes (Indo-1 and Boc-leu-met-MAC), we demonstrated that RGD120 added to prefusing myoblast cultures accelerates myoblast fusion into myotubes, induced an increase of cytosolic free calcium concentration, and concomitantly an increase of intracellular calpain protease activity. Altogether, these results suggested that the efficiency of RGD120 in stimulating myogenesis might be in part explained through its effect on calcium mobilization as well as on the calpain amount and activity. © 2005 Wiley-Liss, Inc. [source] Relative roles of TGF-,1 and Wnt in the systemic regulation and aging of satellite cell responsesAGING CELL, Issue 6 2009Morgan E. Carlson Summary Muscle stem (satellite) cells are relatively resistant to cell-autonomous aging. Instead, their endogenous signaling profile and regenerative capacity is strongly influenced by the aged P-Smad3, differentiated niche, and by the aged circulation. With respect to muscle fibers, we previously established that a shift from active Notch to excessive transforming growth factor-beta (TGF-,) induces CDK inhibitors in satellite cells, thereby interfering with productive myogenic responses. In contrast, the systemic inhibitor of muscle repair, elevated in old sera, was suggested to be Wnt. Here, we examined the age-dependent myogenic activity of sera TGF-,1, and its potential cross-talk with systemic Wnt. We found that sera TGF-,1 becomes elevated within aged humans and mice, while systemic Wnt remained undetectable in these species. Wnt also failed to inhibit satellite cell myogenicity, while TGF-,1 suppressed regenerative potential in a biphasic fashion. Intriguingly, young levels of TGF-,1 were inhibitory and young sera suppressed myogenesis if TGF-,1 was activated. Our data suggest that platelet-derived sera TGF-,1 levels, or endocrine TGF-,1 levels, do not explain the age-dependent inhibition of muscle regeneration by this cytokine. In vivo, TGF-, neutralizing antibody, or a soluble decoy, failed to reduce systemic TGF-,1 and rescue myogenesis in old mice. However, muscle regeneration was improved by the systemic delivery of a TGF-, receptor kinase inhibitor, which attenuated TGF-, signaling in skeletal muscle. Summarily, these findings argue against the endocrine path of a TGF-,1-dependent block on muscle regeneration, identify physiological modalities of age-imposed changes in TGF-,1, and introduce new therapeutic strategies for the broad restoration of aged organ repair. [source] Skeletal muscle fiber type conversion during the repair of mouse soleus: Potential implications for muscle healing after injuryJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 11 2007Tetsuya Matsuura Abstract We used a mouse model of cardiotoxin injury to examine fiber type conversion during muscle repair. We evaluated the soleus muscles of 37 wild-type mice at 2, 4, 8, and 12 weeks after injury. We also used antibodies (fMHC and sMHC) against fast and slow myosin heavy chain to classify the myofibers into three categories: fast-, slow-, and mixed (hybrid)-type myofibers (myofibers expressing both fMHC and sMHC). Our results revealed an increase in the percentage of slow-type myofibers and a decrease in the percentage of fast-type myofibers during the repair process. The percentage of hybrid-type myofibers increased 2 weeks after injury, then gradually decreased over the following 6 weeks. Similarly, our analysis of centronucleated myofibers showed an increase in the percentage of slow-type myofibers and decreases in the percentages of fast- and hybrid-type myofibers. We also investigated the relationship between myofiber type conversion and peroxisome proliferator-activated receptor-, coactivator-1, (PGC-1,). The expression of both PGC-1, protein, which is expressed in both the nucleus and the cytoplasm of regenerating myofibers, and sMHC protein increased with time after cardiotoxin injection, but we observed no significant differential expression of fMHC protein in regenerating muscle fibers during muscle repair. PGC-1,-positive myofibers underwent fast to slow myofiber type conversion during the repair process. These results suggest that PGC-1, contributes to myofiber type conversion after muscle injury and that this phenomenon could influence the recovery of the injured muscle. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1534,1540, 2007 [source] ANABOLIC AGENTS FOR IMPROVING MUSCLE REGENERATION AND FUNCTION AFTER INJURYCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2008Gordon S Lynch SUMMARY 1In the present review, we describe how muscles can be injured by external factors, internal factors or during the performance of some actions during sports. In addition, we describe the injury to a muscle that occurs when its blood supply is interrupted, an occurrence common in clinical settings. An overview of muscle regeneration is presented, as well as a discussion of some of the potential complications that can compromise successful muscle repair and lead to impaired function and permanent disability. 2Improving muscle regeneration is important for hastening muscle repair and restoring muscle function and the present review describes ways in which this can be achieved. We describe recent advances in tissue engineering that offer considerable promise for treating muscle damage, but highlight the fact that these techniques require rigorous evaluation before they can become mainstream clinical treatments. 3Growth-promoting agents are purported to increase the size of existing and newly regenerating muscle fibres and, therefore, could be used to improve muscle function if administered at appropriate times during the repair process. The present review provides an update on the efficacy of some growth-promoting agents, including anabolic steroids, insulin-like growth factor-I (IGF-I) and b2 -adrenoceptor agonists, to improve muscle function after injury. Although these approaches have clinical merit, a better understanding of the androgenic, IGF-I and b-adrenoceptor signalling pathways in skeletal muscle is important if we are to devise safe and effective therapies to enhance muscle regeneration and function after injury. [source] | |||||||||||||