Home About us Contact
|
Home About us Contact | ||
|
|
||
Muscle Regeneration (muscle + regeneration)
Kinds of Muscle Regeneration Selected AbstractsANABOLIC 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] Tissue Repair: Wet-Spun Biodegradable Fibers on Conducting Platforms: Novel Architectures for Muscle Regeneration (Adv. Funct.ADVANCED FUNCTIONAL MATERIALS, Issue 21 2009Mater. Bio-synthetic platforms, consisting of a conducting polymer substrate overlaid with aligned biodegradable fibers promote the linear growth (ex vivo) of partially differentiated muscle fibers, consistent with the structural requirements of skeletal muscle in vivo, as described by J. M. Razal et al. on page 3381. The conducting surface facilitates development of electrical stimulation paradigms for optimizing muscle growth and development ex vivo that may potentially be applied to repair diseased or damaged muscle. [source] Wet-Spun Biodegradable Fibers on Conducting Platforms: Novel Architectures for Muscle RegenerationADVANCED FUNCTIONAL MATERIALS, Issue 21 2009Joselito M. Razal Abstract Novel biosynthetic platforms supporting ex vivo growth of partially differentiated muscle cells in an aligned linear orientation that is consistent with the structural requirements of muscle tissue are described. These platforms consist of biodegradable polymer fibers spatially aligned on a conducting polymer substrate. Long multinucleated myotubes are formed from differentiation of adherent myoblasts, which align longitudinally to the fiber axis to form linear cell-seeded biosynthetic fiber constructs. The biodegradable polymer fibers bearing undifferentiated myoblasts can be detached from the substrate following culture. The ability to remove the muscle cell-seeded polymer fibers when required provides the means to use the biodegradable fibers as linear muscle-seeded scaffold components suitable for in vivo implantation into muscle. These fibers are shown to promote differentiation of muscle cells in a highly organized linear unbranched format in vitro and thereby potentially facilitate more stable integration into recipient tissue, providing structural support and mechanical protection for the donor cells. In addition, the conducting substrate on which the fibers are placed provides the potential to develop electrical stimulation paradigms for optimizing the ex vivo growth and synchronization of muscle cells on the biodegradable fibers prior to implantation into diseased or damaged muscle tissue. [source] Co-expression of IGF-1 family members with myogenic regulatory factors following acute damaging muscle-lengthening contractions in humansTHE JOURNAL OF PHYSIOLOGY, Issue 22 2008Bryon R. McKay Muscle regeneration following injury is dependent on the ability of muscle satellite cells to activate, proliferate and fuse with damaged fibres. This process is controlled by the myogenic regulatory factors (MRF). Little is known about the temporal relation of the MRF with the expression of known myogenic growth factors (i.e. IGF-1) in humans following muscle damage. Eight subjects (20.6 ± 2.1 years; 81.4 ± 9.8 kg) performed 300 lengthening contractions (180 deg s,1) of their knee extensors in one leg on a dynamometer. Blood and muscle samples were collected before and at 4 (T4), 24 (T24), 72 (T72) and 120 h (T120) post-exercise. Mechano growth factor (MGF), IGF-1Ea and IGF-1Eb mRNA were quantified. Serum IGF-1 did not change over the post-exercise time course. IGF-1Ea and IGF-1Eb mRNA increased ,4- to 6-fold by T72 (P < 0.01) and MGF mRNA expression peaked at T24 (P= 0.005). MyoD mRNA expression increased ,2-fold at T4 (P < 0.05). Myf5 expression peaked at T24 (P < 0.05), while MRF4 and myogenin mRNA expression peaked at T72 (P < 0.05). Myf5 expression strongly correlated with the increase in MGF mRNA (r2= 0.83; P= 0.03), while MRF4 was correlated with both IGF-1Ea and -Eb (r2= 0.90; r2= 0.81, respectively; P < 0.05). Immunofluorescence analysis showed IGF-1 protein expression localized to satellite cells at T24, and to satellite cells and the myofibre at T72 and T120; IGF-1 was not detected at T0 or T4. These results suggest that the temporal response of MGF is probably related to the activation/proliferation phase of the myogenic programme as marked by an increase in both Myf5 and MyoD, while IGF-1Ea and - Eb may be temporally related to differentiation as marked by an increase in MRF4 and myogenin expression following acute muscle damage. [source] Muscle stem cells and model systems for their investigationDEVELOPMENTAL DYNAMICS, Issue 12 2007Nicolas Figeac Abstract Stem cells are characterized by their clonal ability both to generate differentiated progeny and to undergo self-renewal. Studies of adult mammalian organs have revealed stem cells in practically every tissue. In the adult skeletal muscle, satellite cells are the primary muscle stem cells, responsible for postnatal muscle growth, hypertrophy, and regeneration. In the past decade, several molecular markers have been found that identify satellite cells in quiescent and activated states. However, despite their prime importance, surprisingly little is known about the biology of satellite cells, as their analysis was for a long time hampered by a lack of genetically amenable experimental models where their properties can be dissected. Here, we review how the embryonic origin of satellite cells was discovered using chick and mouse model systems and discuss how cells from other sources can contribute to muscle regeneration. We present evidence for evolutionarily conserved properties of muscle stem cells and their identification in lower vertebrates and in the fruit fly. In Drosophila, muscle stem cells called adult muscle precursors (AMP) can be identified in embryos and in larvae by persistent expression of a myogenic basic helix,loop,helix factor Twist. AMP cells play a crucial role in the Drosophila life cycle, allowing de novo formation and regeneration of adult musculature during metamorphosis. Based on the premise that AMPs represent satellite-like cells of the fruit fly, important insight into the biology of vertebrate muscle stem cells can be gained from genetic analysis in Drosophila. Developmental Dynamics 236:3332,3342, 2007. © 2007 Wiley-Liss, Inc. [source] Resolution of skeletal muscle inflammation in mdx dystrophic mouse is accompanied by increased immunoglobulin and interferon-, productionINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 3 2002Jussara Lagrota-Candido Summary. Mdx mouse, the animal model of Duchenne muscular dystrophy, develops an X-linked recessive inflammatory myopathy with an apparent sustained capacity for muscle regeneration. We analysed whether changes in the skeletal muscle during myonecrosis and regeneration would correlate with functional alterations in peripheral lymphoid tissues. Here we show that during the height of myonecrosis, mdx mice display marked atrophy of peripheral lymph nodes and extensive muscle inflammation. In contrast, enlargement of draining lymph nodes with accumulation of CD4+ CD44+, CD4+ CD25+, CD8+ CD44+ T lymphocytes and type-2 B cells was consistently observed during amelioration of the muscle lesion. In addition, regeneration of the muscular tissue was accompanied by concomitant increase of immunoglobulin-secreting cells in regional lymph nodes and bone marrow. Double immunolabelling analysis revealed intense B cell proliferation and formation of germinal centre in the follicles of dystrophic regional lymph nodes. Furthermore, lymph node cells produced large amounts of IFN-, but not IL-4, IL-6 or IL-10 after in vitro mitogen stimulation with Concanavalin A. As these alterations occurred mainly during the recovery period, we suggested that local activation of the immune system could be an influence which mitigates the myonecrosis of muscular tissue in the mdx dystrophic mouse. [source] Changing concepts of bladder regenerationINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2007Akihiro Kanematsu Abstract: During the last decade, there has been a dramatic increase in studies aimed at regeneration of the urinary bladder. Many studies employed animal-derived or synthetic materials as grafts for experimental bladder augmentation models, with or without additional measures to promote regeneration, such as autologous cell transplantation or growth factor loading. However, in spite of encouraging results in several reports, few methodologies have shown proven definitive clinical utility. One major problem in these studies is the lack of a clear distinction between native and regenerated bladder in total bladder function after augmentation. Another crucial problem is the absorption and shrinkage of larger grafts, which may result from insufficient vascular supply and smooth muscle regeneration. In contrast, researchers have recently attempted to establish alternative regenerative strategies for treating bladder diseases, and have employed far more diverse approaches according to the various pathological conditions to be treated. For total replacement of the bladder after cystectomy for invasive bladder cancer, urothelium-covered neobladder with non-urinary tract backbone remains a viable choice. In addition, functional bladder diseases such as urinary incontinence, weak detrusor, or non-compliant fibrotic bladder have also been major targets for many leading research groups in this field. These conditions are studied much more from different therapeutic standpoints, aiming at the prevention or reversal of pathological conditions in muscle remodeling or neural control. Such altered research direction would inevitably lead to less surgically based basic biological research, and also would include a far wider spectrum of adult and pediatric bladder diseases, from overactive bladder to dysfunctional voiding. [source] Dermatan sulfate exerts an enhanced growth factor response on skeletal muscle satellite cell proliferation and migrationJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2004Joan Villena Skeletal muscle regeneration is a complex process in which many agents are involved. When skeletal muscle suffers an injury, quiescent resident myoblasts called satellite cells are activated to proliferate, migrate, and finally differentiate. This whole process occurs in the presence of growth factors, the extracellular matrix (ECM), and infiltrating macrophages. We have shown previously that different proteoglycans, either present at the plasma membrane or the ECM, are involved in the differentiation process by regulating growth factor activity. In this article, we evaluated the role of glycosaminoglycans (GAGs) in myoblast proliferation and migration, using C2C12, a satellite cell-derived cell line. A synergic stimulatory effect on myoblast proliferation was observed with hepatocyte growth factor (HGF) and fibroblast growth factor type 2 (FGF-2), which was dependent on cell sulfation. The GAG dermatan sulfate (DS) enhanced HGF/FGF-2-dependent proliferation at 1,10 ng/ml. However, decorin, a proteoglycan containing DS, was unable to reproduce this enhanced proliferative effect. On the other hand, HGF strongly increased myoblast migration. The HGF-dependent migratory process required the presence of sulfated proteoglycans/GAGs present on the myoblast surface, as inhibition of both cell sulfation, and heparitinase (Hase) and chondroitinase ABC (Chabc) treatment of myoblasts, resulted in a very strong inhibition of cell migration. Among the GAGs analyzed, DS most increased HGF-dependent myoblast migration. Taken together, these findings showed that DS is an enhancer of growth factor-dependent proliferation and migration, two critical processes involved in skeletal muscle formation. J. Cell. Physiol. 198: 169,178, 2004© 2003 Wiley-Liss, Inc. [source] Skeletal muscle regeneration: report of a case presenting as a cutaneous nodule following blunt trauma to the lipJOURNAL OF CUTANEOUS PATHOLOGY, Issue 4 2007Samer H. Ghosn A 61-year-old man presented with a 4-month history of an enlarging nodule on the upper lip following blunt trauma. An initial punch biopsy was non-diagnostic. A deeper biopsy revealed a multilobular proliferation of atypical and pleomorphic cells with vesicular nuclei, prominent nucleoli, and large amphophilic cytoplasm. Immunoperoxidase studies showed these cells to be positive for muscle-specific actin and desmin and negative for S-100 protein and smooth muscle actin. Based on these findings, a diagnosis of skeletal muscle regeneration (SMR) was made. To our knowledge, this is the first report of SMR presenting clinically as a rapidly growing cutaneous nodule on the lip following blunt trauma. [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] Long-term morphometric and immunohistochemical findings in human free microvascular muscle flaps,MICROSURGERY, Issue 1 2004M. Susanna C. Kauhanen M.D., Ph.D. Reinnervation, muscle regeneration, density of microvessels, and muscle-type specific atrophy were studied 3,4 years after surgery in surgically nonreinnervated free microvascular muscle flaps to 13 patients transplanted to the upper or lower extremities. Routine histology and immunohistochemistry for PGP 9.5 and S-100 (neuronal markers), Ki-67 (cell proliferation), myosin (muscle fiber types), and CD-31 (endothelium) were carried out, and results were analyzed morphometrically. Three to 4 years after surgery, severe atrophy of predominantly slow-type fibers was seen in 9 cases. In 4 cases, muscle-fiber diameter and fiber-type distribution were close to normal. Long intraoperative muscle ischemia and postoperative immobilization were associated with poor muscle bulk in flaps. The density of microvessels in flaps did not differ from control muscles. PGP 9.5 and S-100 immunopositive nerve fibers were detected in 7 patients. Reinnervation was associated with good muscle bulk. In 4 patients, activation of satellite cells was evident. The results suggest that in some cases, spontaneous reinnervation may occur in free muscle flaps, and that several years after microvascular free flap transfer, the muscle still attempts to regenerate. © 2004 Wiley-Liss, Inc. [source] Improvement of muscle healing through enhancement of muscle regeneration and prevention of fibrosisMUSCLE AND NERVE, Issue 3 2003Kenji Sato MD Abstract Skeletal muscle is able to repair itself through regeneration. However, an injured muscle often does not fully recover its strength because complete muscle regeneration is hindered by the development of fibrosis. Biological approaches to improve muscle healing by enhancing muscle regeneration and reducing the formation of fibrosis are being investigated. Previously, we have determined that insulin-like growth factor,1 (IGF-1) can improve muscle regeneration in injured muscle. We also have investigated the use of an antifibrotic agent, decorin, to reduce muscle fibrosis following injury. The aim of this study was to combine these two therapeutic methods in an attempt to develop a new biological approach to promote efficient healing and recovery of strength after muscle injuries. Our findings indicate that further improvement in the healing of muscle lacerations is attained histologically by the combined administration of IGF-1 to enhance muscle regeneration and decorin to reduce the formation of fibrosis. This improvement was not associated with improved responses to physiological testing, at least at the time-points tested in this study. Muscle Nerve 28: 365,372, 2003 [source] The expression pattern of PKC, in satellite cells of normal and regenerating muscle in the ratNEUROPATHOLOGY, Issue 3 2009Seiji Tokugawa Protein kinase C (PKC) is a key enzyme in regulating a variety of cellular functions. PKC, is the most abundant PKC isoform expressed in skeletal muscle. However, the functional role of PKC, linked to muscle regeneration has not yet been identified. Using reverse transcription (RT)-PCR and immunofluorescence analysis, we investigated the expression patterns of PKC, in normal and regenerating tibialis anterior (TA) muscles in the rat. The amount of PKC, mRNA in the muscle increased from the 4th to 6th post-surgical day. Immunofluorescence revealed PKC, protein in quiescent satellite cells identified by c-Met. PKC, immunoreactivity was not observed in many proliferating satellite cells by labeling with BrdU in the regenerating muscle. At 4, 6 and 10 days postsurgery, PKC, immunoreactivity was observed in half the differentiating satellite cells labeling with myogenin. After 4 and 6 days, the localization of PKC, coincided with those of Pax7 and TGF-,. Thus, PKC, may play an important role in inhibiting differentiation and maintaining the quiescent satellite cells in muscle regeneration. [source] Expression of the dermatomyositis autoantigen Mi-2 in regenerating muscleARTHRITIS & RHEUMATISM, Issue 12 2009Andrew L. Mammen Objective Autoantibodies against the chromatin remodeler Mi-2 are found in a distinct subset of patients with dermatomyositis (DM). Previous quantitative immunoblotting experiments demonstrated that Mi-2 protein levels are up-regulated in DM muscle. This study was undertaken to define the population of cells expressing high levels of Mi-2 in DM muscle and to explore the regulation and functional role of Mi-2 during muscle regeneration. Methods The expression of Mi-2 was analyzed by immunofluorescence microscopy in human muscle biopsy specimens. In an experimental mouse model, cardiotoxin was used to induce muscle injury and repair, and expression of Mi-2 during muscle regeneration was studied in this model by immunofluorescence and immunoblotting analyses. In addition, a cell culture system of muscle differentiation was utilized to artificially modulate Mi-2 levels during proliferation and differentiation of myoblasts. Results In human DM muscle tissue, increased Mi-2 expression was found preferentially in the myofibers within fascicles affected by perifascicular atrophy, particularly in the centralized nuclei of small perifascicular muscle fibers expressing markers of regeneration. In injured mouse muscle tissue, Mi-2 levels were dramatically and persistently up-regulated during muscle regeneration in vivo. Premature silencing of Mi-2 with RNA interference in vitro resulted in accelerated myoblast differentiation. Conclusion Expression of Mi-2 is markedly up-regulated during muscle regeneration in a mouse model of muscle injury and repair. It is also up-regulated in human DM myofibers expressing markers of regeneration. Results of the in vitro studies indicate that this protein may play a role in modulating the kinetics of myoblast differentiation. Our findings thus suggest that high levels of Mi-2 expression in muscle biopsy tissue from patients with DM reflect the presence of incompletely differentiated muscle cells. [source] Novel role for ,-adrenergic signalling in skeletal muscle growth, development and regenerationCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2010James G Ryall Summary 1. In adult mammals, skeletal muscle mass is maintained through a precise balance of protein synthesis and protein degradation, whereas during development cellular (not protein) turnover predominates. When protein balance is shifted towards synthesis, skeletal muscle hypertrophy ensues. In contrast, increased protein degradation leads to skeletal muscle atrophy. Insulin-like growth factor (IGF)-I is among the best documented of the growth factors and regulates skeletal muscle mass by increasing protein synthesis and decreasing protein degradation. However, an IGF-I-independent growth pathway has been identified that involves the activation of ,-adrenoceptors and subsequent skeletal muscle growth, development and hypertrophy. 2. Although the importance of ,-adrenergic signalling in the heart has been well documented and continues to receive significant attention, it is only more recently that we have started to appreciate the importance of this signalling pathway in skeletal muscle structure and function. Studies have identified an important role for ,-adrenoceptors in myogenesis and work from our laboratory has identified a novel role for ,-adrenoceptors in regulating skeletal muscle regeneration after myotoxic injury. In addition, new data suggest that ,-adrenoceptors are markedly upregulated during differentiation of C2C12 cells. 3. It is now clear that ,-adrenoceptors play an important role in regulating skeletal muscle structure and function. Importantly, a clearer understanding of the pathways regulating skeletal muscle mass may lead to the identification of novel therapeutic targets for the treatment of muscle wasting disorders, including sarcopenia, cancer cachexia and the muscular dystrophies. [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] USE OF PORCINE SMALL INTESTINAL SUBMUCOSA IN BLADDER AUGMENTATION IN RABBIT: LONG-TERM HISTOLOGICAL OUTCOMEANZ JOURNAL OF SURGERY, Issue 1-2 2008Ali Ayyildiz Aim: To investigate long-term histological features of bladder augmentation using porcine small intestine submucosa (SIS) in a rabbit model. Materials and method: Sixteen New Zealand rabbits were used. Porcine SIS was provided by a manufactured formation derived from the pig. After partial cystectomy was carried out on the bladder, a single layer of SIS (Cook® -SIS Technology, Cook Biotech Incorporated, West Lafayette, IN, USA) (2 × 5 cm) was sewn to bladder with continuous 5/0 vicryl suture material in a watertight manner. Urinary diversion was not used. The rabbits were killed 12 months later and perivesical fat was removed together with bladder. The 5-,m preparations taken from the samples were stained with haematoxylin,eosin and Mason's trichrome dye. S-100 and F8 stains were also used for immunohistochemical investigations. Results: The macroscopic view of bladder was normal. SIS was indistinguishable from normal bladder wall, but the region of the graft had a slight white coloration. Microscopic observations showed the continuity of transitional epithelium of host bladder tissue on SIS material. Detrusor and serosal layers were formed and these layers were indistinguishable from host bladder. Fibroblasts were scattered among the collagen fibrils. New vessel formations were present without lymphatic proliferation. Nerve regeneration was excellent. No inflammation was observed in normal and regenerated bladder wall. Conclusion: At the end of 12 months, the long-term histological features of bladder augmentation with porcine SIS in a rabbit model, such as presence of new vessel formations, nerve regeneration, collagen and smooth muscle regenerations, which were indistinguishable from original bladder, and the absence of inflammation, showed that SIS seems to be a viable alternative to the use of intestine in bladder augmentation. [source] | |||||||||||||