Relevant bibliographies by topics / Muscle regeneration

Academic literature on the topic 'Muscle regeneration'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Muscle regeneration"

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Kami, Katsuya, and Emiko Senba. "In Vivo Activation of STAT3 Signaling in Satellite Cells and Myofibers in Regenerating Rat Skeletal Muscles." Journal of Histochemistry & Cytochemistry 50, no. 12 (December 2002): 1579–89. http://dx.doi.org/10.1177/002215540205001202.

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Although growth factors and cytokines play critical roles in skeletal muscle regeneration, intracellular signaling molecules that are activated by these factors in regenerating muscles have been not elucidated. Several lines of evidence suggest that leukemia inhibitory factor (LIF) is an important cytokine for the proliferation and survival of myoblasts in vitro and acceleration of skeletal muscle regeneration. To elucidate the role of LIF signaling in regenerative responses of skeletal muscles, we examined the spatial and temporal activation patterns of an LIF-associated signaling molecule, the signal transducer and activator transcription 3 (STAT3) proteins in regenerating rat skeletal muscles induced by crush injury. At the early stage of regeneration, activated STAT3 proteins were first detected in the nuclei of activated satellite cells and then continued to be activated in proliferating myoblasts expressing both PCNA and MyoD proteins. When muscle regeneration progressed, STAT3 signaling was no longer activated in differentiated myoblasts and myotubes. In addition, activation of STAT3 was also detected in myonuclei within intact sarcolemmas of surviving myofibers that did not show signs of necrosis. These findings suggest that activation of STAT3 signaling is an important molecular event that induces the successful regeneration of injured skeletal muscles.
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2

Gulati, Adarshk. "Pattern of skeletal muscle regeneration after reautotransplantation of regenerated muscle." Development 92, no. 1 (March 1, 1986): 1–10. http://dx.doi.org/10.1242/dev.92.1.1.

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Autotransplantation of rat extensor digitorum longus muscle results in initial myofibre degeneration and subsequent regeneration from precursor myosatellite cells. To determine what effect a reinjury would have on the regenerative response, in the present,study, once transplanted and regenerated muscles were reinjured by reautotransplantion. In rats, four weeks after initial transplantation, when the regeneration was complete, the extensor digitorum longus muscle was transplanted again and the pattern of regeneration in reautotransplanted and once auto transplanted muscles was compared. Muscles were analysed 2, 4, 7, 14 and 30 days after autotransplantation and reautotransplantation. Both autotransplanted and reautotransplanted muscles underwent degeneration and regeneration; however, the pattern of regeneration in these two transplants was quite different. In autotransplants, a thin myogenic zone, marked by activated myoblasts, was first seen at 4 days. By 7 days the width of myogenic zone increased but still many degenerating myofibres were present in the central region of the muscle. By 14 days the muscle was filled with regenerated myotubes and myofibres. The reautotransplanted muscles underwent similar regenerative events; however, the rate of regeneration was considerably faster. The myogenic zone was apparent as early as 2 days and was much larger at 4 days, and by 7 days the entire muscle was filled with regenerated myotubes and myofibres which matured at later time intervals. Furthermore, the decrease in muscle weight in reautotransplanted muscles was not as much as that seen after autotransplantation. These findings reveal that not only is skeletal muscle capable of regeneration after a second injury, but the rate of this regeneration is much faster. This increased rate and recovery may be due to a conditioning effect of the first injury.
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Carlsen, R. C., D. Kerlin, and S. D. Gray. "Regeneration and revascularization of a nerve-intact skeletal muscle graft in the spontaneously hypertensive rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 1 (January 1, 1996): R153—R161. http://dx.doi.org/10.1152/ajpregu.1996.270.1.r153.

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Skeletal muscles in hypertensive subjects develop an increased resistance to insulin that reduces their ability to incorporate glucose and synthesize glycogen. Insulin is an anabolic hormone in muscle, and muscle insulin receptors bind the growth factor, insulin-like growth factor I (IGF-I), an important contributor to muscle development and regeneration. An increase in insulin resistance in hypertensive subjects might produce muscle atrophy and weakness or limit regenerative growth after injury. Regenerative muscle growth was assessed in 24-to 26-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats by subjecting extensor digitorum longus (EDL), an ankle flexor, to a nerve-intact graft procedure. The procedure produces extensive muscle fiber and capillary degeneration, but has little effect on the muscle nerve. Muscle morphology and contractile function were examined in intact and regenerating EDL at 21, 42, and 63 days postgraft. Muscle revascularization was assessed histologically at the same time points. Severe established hypertension did not prevent the reestablishment of a structurally normal capillary network in injured muscles. SHR muscle fiber regeneration and maturation, however, were significantly depressed compared with WKY grafts. The reduced regenerative recovery of SHR EDL in adult animals with severe hypertension does not appear to be due to a failure to restore the muscle nerve or capillary network, but may reflect a reduced anabolic response to insulin or IGF-I.
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Zimowska, Małgorzata, Karolina Archacka, Edyta Brzoska, Joanna Bem, Areta M. Czerwinska, Iwona Grabowska, Paulina Kasprzycka, et al. "IL-4 and SDF-1 Increase Adipose Tissue-Derived Stromal Cell Ability to Improve Rat Skeletal Muscle Regeneration." International Journal of Molecular Sciences 21, no. 9 (May 7, 2020): 3302. http://dx.doi.org/10.3390/ijms21093302.

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Skeletal muscle regeneration depends on the satellite cells, which, in response to injury, activate, proliferate, and reconstruct damaged tissue. However, under certain conditions, such as large injuries or myopathies, these cells might not sufficiently support repair. Thus, other cell populations, among them adipose tissue-derived stromal cells (ADSCs), are tested as a tool to improve regeneration. Importantly, the pro-regenerative action of such cells could be improved by various factors. In the current study, we tested whether IL-4 and SDF-1 could improve the ability of ADSCs to support the regeneration of rat skeletal muscles. We compared their effect at properly regenerating fast-twitch EDL and poorly regenerating slow-twitch soleus. To this end, ADSCs subjected to IL-4 and SDF-1 were analyzed in vitro and also in vivo after their transplantation into injured muscles. We tested their proliferation rate, migration, expression of stem cell markers and myogenic factors, their ability to fuse with myoblasts, as well as their impact on the mass, structure and function of regenerating muscles. As a result, we showed that cytokine-pretreated ADSCs had a beneficial effect in the regeneration process. Their presence resulted in improved muscle structure and function, as well as decreased fibrosis development and a modulated immune response.
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Banerji, Christopher R. S., Don Henderson, Rabi N. Tawil, and Peter S. Zammit. "Skeletal muscle regeneration in facioscapulohumeral muscular dystrophy is correlated with pathological severity." Human Molecular Genetics 29, no. 16 (August 3, 2020): 2746–60. http://dx.doi.org/10.1093/hmg/ddaa164.

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Abstract Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal-dominant myopathy characterized by slowly progressive skeletal muscle weakness and wasting. While a regenerative response is often provoked in many muscular dystrophies, little is known about whether a regenerative response is regularly elicited in FSHD muscle, prompting this study. For comparison, we also examined the similarly slowly progressing myotonic dystrophy type 2 (DM2). To first investigate regeneration at the transcriptomic level, we used the 200 human gene Hallmark Myogenesis list. This myogenesis biomarker was elevated in FSHD and control healthy myotubes compared to their myoblast counterparts, so is higher in myogenic differentiation. The myogenesis biomarker was also elevated in muscle biopsies from most independent FSHD, DM2 or Duchenne muscular dystrophy (DMD) studies compared to control biopsies, and on meta-analysis for each condition. In addition, the myogenesis biomarker was a robust binary discriminator of FSHD, DM2 and DMD from controls. We also analysed muscle regeneration at the protein level by immunolabelling muscle biopsies for developmental myosin heavy chain. Such immunolabelling revealed one or more regenerating myofibres in 76% of FSHD muscle biopsies from quadriceps and 91% from tibialis anterior. The mean proportion of regenerating myofibres per quadriceps biopsy was 0.48%, significantly less than 1.72% in the tibialis anterior. All DM2 muscle biopsies contained regenerating myofibres, with a mean of 1.24% per biopsy. Muscle regeneration in FSHD was correlated with the pathological hallmarks of fibre size variation, central nucleation, fibrosis and necrosis/regeneration/inflammation. In summary, the regenerative response in FSHD muscle biopsies correlates with the severity of pathology.
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Dadgar, Sherry, Zuyi Wang, Helen Johnston, Akanchha Kesari, Kanneboyina Nagaraju, Yi-Wen Chen, D. Ashley Hill, et al. "Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy." Journal of Cell Biology 207, no. 1 (October 13, 2014): 139–58. http://dx.doi.org/10.1083/jcb.201402079.

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We sought to determine the mechanisms underlying failure of muscle regeneration that is observed in dystrophic muscle through hypothesis generation using muscle profiling data (human dystrophy and murine regeneration). We found that transforming growth factor β–centered networks strongly associated with pathological fibrosis and failed regeneration were also induced during normal regeneration but at distinct time points. We hypothesized that asynchronously regenerating microenvironments are an underlying driver of fibrosis and failed regeneration. We validated this hypothesis using an experimental model of focal asynchronous bouts of muscle regeneration in wild-type (WT) mice. A chronic inflammatory state and reduced mitochondrial oxidative capacity are observed in bouts separated by 4 d, whereas a chronic profibrotic state was seen in bouts separated by 10 d. Treatment of asynchronously remodeling WT muscle with either prednisone or VBP15 mitigated the molecular phenotype. Our asynchronous regeneration model for pathological fibrosis and muscle wasting in the muscular dystrophies is likely generalizable to tissue failure in chronic inflammatory states in other regenerative tissues.
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Launay, Thierry, Philippe Noirez, Gillian Butler-Browne, and Onnik Agbulut. "Expression of slow myosin heavy chain during muscle regeneration is not always dependent on muscle innervation and calcineurin phosphatase activity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 6 (June 2006): R1508—R1514. http://dx.doi.org/10.1152/ajpregu.00486.2005.

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In the literature, there is an ambiguity as to the respective roles played by calcineurin phosphatase activity (CPA) and muscle innervation in the reestablishment of the slow-twitch muscle phenotype after muscle regeneration in different species. In this study, we wanted to determine the role of calcineurin and muscle innervation on the appearance and maintenance of the slow phenotype during mouse muscle regeneration. The pattern of myosin expression and CPA was analyzed in adult ( n = 15), regenerating ( n = 45) and denervated-regenerating ( n = 32) slow-twitch soleus and fast-twitch extensor digitorum longus (EDL) muscles. Moreover, in a second group of denervated-regenerating mice ( n = 9), the animals were treated with a calcineurin inhibitor. Regeneration was induced by injection of cardiotoxin and in the denervated-regenerating group, denervation was carried out by cutting the sciatic nerve before the administration of cardiotoxin. In innervated-regenerating soleus muscle, CPA increased continuously after 10 days postinjury and by 21 days, there was a 3.5-fold increase in CPA compared with adult basal level, whereas in innervated-regenerating EDL muscle, CPA remained unchanged. Moreover, our results show that in denervated-regenerating muscles, the MyHC profile was identical in spite of the functional differences inherent in these muscles. In long-term denervated-regenerating muscles, a slow muscle phenotype was reexpressed both in the presence or absence of calcineurin inhibitor. Our results show that although in innervated-regenerating mouse muscle, the appearance of a slow phenotype is correlated with a peak of CPA, in denervated-regenerating muscles, a slow phenotype is triggered and maintained in a calcineurin- and nerve-independent manner.
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Zullo, Letizia, Matteo Bozzo, Alon Daya, Alessio Di Clemente, Francesco Paolo Mancini, Aram Megighian, Nir Nesher, et al. "The Diversity of Muscles and Their Regenerative Potential across Animals." Cells 9, no. 9 (August 19, 2020): 1925. http://dx.doi.org/10.3390/cells9091925.

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Cells with contractile functions are present in almost all metazoans, and so are the related processes of muscle homeostasis and regeneration. Regeneration itself is a complex process unevenly spread across metazoans that ranges from full-body regeneration to partial reconstruction of damaged organs or body tissues, including muscles. The cellular and molecular mechanisms involved in regenerative processes can be homologous, co-opted, and/or evolved independently. By comparing the mechanisms of muscle homeostasis and regeneration throughout the diversity of animal body-plans and life cycles, it is possible to identify conserved and divergent cellular and molecular mechanisms underlying muscle plasticity. In this review we aim at providing an overview of muscle regeneration studies in metazoans, highlighting the major regenerative strategies and molecular pathways involved. By gathering these findings, we wish to advocate a comparative and evolutionary approach to prompt a wider use of “non-canonical” animal models for molecular and even pharmacological studies in the field of muscle regeneration.
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Anderson, Judy E., Laura M. McIntosh, Andrea N. Moor (neé Pernitsky), and Zipora Yablonka–Reuveni. "Levels of MyoD Protein Expression Following Injury of mdx and Normal Limb Muscle Are Modified by Thyroid Hormone." Journal of Histochemistry & Cytochemistry 46, no. 1 (January 1998): 59–67. http://dx.doi.org/10.1177/002215549804600108.

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Thyroid hormone (T3) affects muscle development and muscle regeneration. It also interacts with the muscle regulatory gene MyoD in culture and affects myoblast proliferation. We studied the localization of MyoD protein using a well-characterized polyclonal antibody for immunohistochemistry. Relative numbers of myogenic precursor cells per field were identified by their MyoD expression during muscle regeneration in normal and mdx dystrophic mice, with particular reference to the expression in mononuclear cells and myotubes at various T3 levels. In regeneration by normal muscles, relatively few MyoD+ nuclei per field were present in mononuclear cells of euthyroid and hypothyroid mice. MyoD staining of mononuclear cell nuclei was approximately doubled in fields of regenerating muscles of normal hyperthyroid compared to euthyroid mice, and was observed in precursors that appeared to be aligned before fusion into myotubes. In mdx regenerating muscle, twofold more mononuclear cells positive for MyoD were present in all three treatment groups compared to normal muscles regenerating under the same conditions. Localization was similar to the pattern in normal euthyroid mice. However, in muscles regenerating in hyperthyroid mdx mice, both mononuclear cell nuclei and centrally located nuclei in a subpopulation (about 15%) of new myotubes formed after the crush injury were intensely stained for MyoD protein. The changes observed are consistent with reports on T3-induced alteration of muscle repair, and propose a link between MyoD regulation and the accelerated differentiation during regeneration under high T3 conditions.
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Rahman, Fasih Ahmad, Sarah Anne Angus, Kyle Stokes, Phillip Karpowicz, and Matthew Paul Krause. "Impaired ECM Remodeling and Macrophage Activity Define Necrosis and Regeneration Following Damage in Aged Skeletal Muscle." International Journal of Molecular Sciences 21, no. 13 (June 27, 2020): 4575. http://dx.doi.org/10.3390/ijms21134575.

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Regenerative capacity of skeletal muscle declines with age, the cause of which remains largely unknown. We investigated extracellular matrix (ECM) proteins and their regulators during early regeneration timepoints to define a link between aberrant ECM remodeling, and impaired aged muscle regeneration. The regeneration process was compared in young (three month old) and aged (18 month old) C56BL/6J mice at 3, 5, and 7 days following cardiotoxin-induced damage to the tibialis anterior muscle. Immunohistochemical analyses were performed to assess regenerative capacity, ECM remodeling, and the macrophage response in relation to plasminogen activator inhibitor-1 (PAI-1), matrix metalloproteinase-9 (MMP-9), and ECM protein expression. The regeneration process was impaired in aged muscle. Greater intracellular and extramyocellular PAI-1 expression was found in aged muscle. Collagen I was found to accumulate in necrotic regions, while macrophage infiltration was delayed in regenerating regions of aged muscle. Young muscle expressed higher levels of MMP-9 early in the regeneration process that primarily colocalized with macrophages, but this expression was reduced in aged muscle. Our results indicate that ECM remodeling is impaired at early time points following muscle damage, likely a result of elevated expression of the major inhibitor of ECM breakdown, PAI-1, and consequent suppression of the macrophage, MMP-9, and myogenic responses.
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Dissertations / Theses on the topic "Muscle regeneration"

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Pillitteri, Paul J. "Regeneration of Rat Skeletal Muscle Following a Muscle Biopsy." Ohio University / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1118087917.

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Nearing, Marie. "The Role of the Regenerating Protein Family on Skeletal Muscle Regeneration." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/268516.

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Skeletal muscle regeneration is dependent upon the influences of intrinsic and extrinsic factors that stimulate satellite cells. Regenerating proteins are upregulated at the onset of trauma or inflammation in the pancreas, gastrointestinal tract, liver, neural cells and other tissues. Studies have shown that Reg proteins have a mitogenic, anti-apoptotic and anti-inflammatory function in damaged tissues and is necessary for normal progression of regeneration. As skeletal muscle is also able to regenerate itself at a rapid rate, it seems highly likely that Reg proteins function to promote myogenesis in skeletal muscle regeneration. Therefore, the goal of our research was to characterize the expression of the Reg proteins and receptor in regenerating skeletal muscle and satellite cells, investigate the effect of exogenous Reg protein on myogenesis, and to examine direct Reg protein effect on satellite cell activity. To determine whether Reg proteins participate in skeletal muscle regeneration, mice were injected with marcaine in their tibialis anterior muscles to induce skeletal muscle damage. The gene expression analysis of undamaged and marcaine-damaged tibialis anterior muscles and mice satellite cells showed that Reg I, II, IIIα, IIIγ, IV and EXTL3 genes are present during skeletal muscle regeneration and satellite cells significantly express Reg I, IIIα, IIIγ and EXTL3. As Reg I and IIIα are most prevalent in vivo and in vitro respectively, we advocate these isoforms as the predominant candidates in skeletal muscle regeneration. To determine the effect of exogenous Reg protein on myogenesis, we performed gene expression and muscle morphometry analysis of Reg IIIα or PBS injected tibialis anterior muscles. Interestingly, our results indicate that the addition of Reg IIIα to damaged muscles inhibited myogenesis. To determine the direct effect of Reg protein on myogenic stem cell activity, Reg proteins were added to mice satellite cells and C2C12 cells. Results from these studies were inconclusive due to the failure of known positive and negative controls. Overall, our studies suggest that Reg proteins contribute to skeletal muscle regeneration; however, as an overabundance of Reg IIIα in regenerating tissues may have inhibited myogenesis, it is imperative that other isoforms or lower concentrations be investigated.
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Baker, Brent A. "Characterization of skeletal muscle performance and morphology following acute and chronic mechanical loading paradigms." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5325.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains xii, 270 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Charge, Sophie Barbara Pauline. "Skeletal muscle hypertrophy : its regulation and effect on muscle regeneration." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340500.

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Dyer, Kelly Anne. "Chracterisation of Mighty during Skeletal Muscle Regeneration." The University of Waikato, 2006. http://hdl.handle.net/10289/2243.

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Satellite cells are a distinct lineage of myogenic precursors that are responsible for the growth of muscle during post-natal life and for its repair after damage. During muscle growth and regeneration satellite cells are activated in response to growth signals from the environment, which induces the expression of one or both of the two MRFs, Myf-5 or MyoD. Activated satellite cells migrate to the site of injury and proliferate before these transcription factors go on to activate transcription of myogenic genes. The myoblasts can then adopt one of two fates. Some myoblasts initiate terminal differentiation and are able to either fuse into existing myofibres to repair them, or fuse with other myoblasts to form new fibres. Other myoblasts do not differentiate but instead return to quiescence and adopt a satellite cell position on repaired or newly formed fibres. Mighty, a downstream target of myostatin that was discovered by the Functional Muscle Genomics Laboratory has recently been shown to induce cell hypertrophy in cell culture through enhanced differentiation and fusion of myoblasts. Myostatin-null mice have hypertrophic muscles and an improved muscle regeneration phenotype. These mice have also been shown to have higher basal levels of Mighty in skeletal muscle than wild-type mice. In this thesis the expression profile of Mighty during skeletal muscle regeneration was characterised in relation to MyoD. During regeneration Mighty gene expression was induced at day five post-injury in both wild-type and myostatin-null mice. In the myostatin-null mice Mighty gene expression remained elevated at day seven post injury in contrast to the levels in the wild-type, which had decreased at this time point. By day-14 and day-28 post-injury Mighty levels were decreased. The up-regulation of Mighty occurs at the time of peak myotube formation in regenerating skeletal muscle, consistent with a role for Mighty in enhancing differentiation and fusion of myoblasts. The extended up-regulation of Mighty in the myostatin-null muscle may be responsible for the enhanced regeneration phenotype of these mice. Analysis of the myotube and reserve cell populations, which are an in vitro model of satellite cells, from both C2C12 cells and Mighty over-expressing clones (Clone 7 and Clone 11) showed that Mighty expression down-regulates two satellite cell markers, CD34 and Sca-1. Both these molecules have been recently shown to be involved in myoblast fusion and reserve cell specification, although their exact role in these processes is not yet known. Expression of Sca-1 is associated with a slowly proliferating non-dividing state while CD34 is associated with the population of reserve cells that do not fuse when notch signalling is inhibited. The results of this thesis indicate that Mighty over-expression may cause the enhanced fusion phenotype by regulating these two molecules. In conclusion the data in this thesis supports a role for Mighty in the myotube formation phase of regeneration and may be able to enhance regeneration by recruiting more myoblasts to terminal differentiation by altering CD34 and Sca-1 expression.
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Markert, Chad D. "Ultrasound and exercise in skeletal muscle regeneration." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1091304498.

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Thesis (Ph. D.)--Ohio State University, 2004.
Document formatted into pages. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 Aug. 2.
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LANGONE, FRANCESCA. "Perturbation of muscle regeneration by small molecules." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202067.

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Skeletal muscle plays fundamental roles for locomotion, posture maintenance and breathing and to preserve its function, skeletal muscle has developed a remarkable capacity to regenerate also after severe damage. Several studies aimed at understanding the cellular and molecular mechanisms involved in muscle repair that are deregulated in muscular dystrophy-associated fibrosis and in aging-related muscle dysfunction. However, the cellular and molecular effectors of muscle repair remain largely unknown. This doctoral thesis aims at understanding molecular mechanisms and the interplay between different muscle populations, by perturbing muscle regeneration and differentiation with small molecules. Recent studies have suggested that muscle regenerative process is improved when AMPK is activated. In the muscle of young and old mice a low calorie diet, which activates AMPK, markedly enhances muscle regeneration. Remarkably, intraperitoneal injection of AICAR, an AMPK agonist, improves the structural integrity of muscles of dystrophin-deficient mdx mice. Building on these observations we asked whether metformin, a powerful anti-hyperglycemic drug, which indirectly activates AMPK, affects the response of skeletal muscle to damage. In our conditions, metformin treatment did not significantly influence muscle regeneration. On the other hand we observed that the muscles of metformin treated mice are more resilient to cardiotoxin injury displaying lesser muscle damage. Accordingly myotubes, originated in vitro from differentiated C2C12 myoblast cell line, become more resistant to cardiotoxin damage after pre-incubation with metformin. Our results indicate that metformin limits cardiotoxin damage by protecting myotubes from necrosis. Although the details of the molecular mechanisms underlying the protective effect remain to be elucidated, we report a correlation between the ability of metformin to promote resistance to damage and its capacity to counteract the increment of intracellular calcium levels induced by cardiotoxin treatment. Since increased cytoplasmic calcium concentrations characterize additional muscle pathological conditions, including dystrophies, metformin treatment could prove a valuable strategy to ameliorate the conditions of patients affected by dystrophies. Moreover, in order to understand and control the differentiation decisions of muscle cell populations, we used automated fluorescence microscopy to screen the Prestwick library of small molecules 100% approved by the U.S. Food and Drug Administration (FDA). We have developed fluorescence microscopy readouts to monitor cell proliferation and differentiation into skeletal muscle, adipocyte or osteoblasts both in mesoangioblasts (MABS), a muscle multipotent cell line, and in a heterogeneous mixture of diverse muscle cell populations. We performed the high-throughput and highcontent screening, in order to identify compounds that either promote or inhibit the differentiation process. To date we have screened 240 molecules and we produced a list of drugs that affect the differentiation of muscle cells in skeletal muscle, adipocytes or osteoblasts. We have performed experiments to validate the list of putative interfering small molecules and in parallel we have built a similarity tree from the collection of transcriptional expression profile data from cultured human cells treated with bioactive small molecules, developed by the Connectivity Map team in The Broad Institute of MIT. By highlighting the obtained putative drugs in the similarity tree, we can discriminate if drugs affecting a specific differentiation phenotype may do so via similar or different molecular pathway and we can identify molecular mechanisms involved in differentiation decision.
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Vidal, Iglesias Berta. "The fibrinolitys system in muscle regeneration and dystrophy." Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7143.

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Duchenne muscular dystrophy (DMD) is a fatal degenerative disorder of locomotor and respiratory muscles, in which myofibers are progressively replaced by non-muscular fibrotic tissue. Here, we show that fibrin/ogen accumulates in dystrophic muscles of DMD patients and of the mdx mouse model of DMD. Genetic loss or pharmacological depletion of fibrin/ogen in mdx mice attenuated muscular dystrophy progression and improved locomotor capacity. More importantly, fibrin/ogen depletion reduced fibrosis in mdx mouse diaphragm. Our data indicate that fibrin/ogen, through induction of IL-1 Ò, drives the synthesis of TGF Ò by mdx macrophages, which in turn, induces collagen production in mdx fibroblasts. Fibrin/ogen-produced TGF Ò further amplifies collagen accumulation through recruitment and activation of pro-fibrotic alternatively activated macrophages. Fibrin/ogen also stimulated collagen synthesis directly in mdx fibroblasts, via Ñv Ò3 integrin engagement. In addition, when analyzing a group of 39 DMD patients, fibrin/ogen accumulation in locomotor muscles was found associated with fibrosis and disease severity. These data unveil a novel role of fibrin/ogen in muscular dystrophy and, importantly, in the replacement of muscle by fibrotic tissue.
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Chang, C. F. "Studies of muscle regeneration in avian muscular dystrophy." Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/38258.

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Grasman, Jonathan M. "Designing Fibrin Microthread Scaffolds for Skeletal Muscle Regeneration." Digital WPI, 2015. https://digitalcommons.wpi.edu/etd-dissertations/18.

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Volumetric muscle loss (VML) typically results from traumatic incidents; such as those presented from combat missions, where soft-tissue extremity injuries account for approximately 63% of diagnoses. These injuries lead to a devastating loss of function due to the complete destruction of large amounts of tissue and its native basement membrane, removing important biochemical cues such as hepatocyte growth factor (HGF), which initiates endogenous muscle regeneration by recruiting progenitor cells. Clinical strategies to treat these injuries consist of autologous tissue transfer techniques, requiring large amounts of healthy donor tissue and extensive surgical procedures that can result in donor site morbidity and limited functional recovery. As such, there is a clinical need for an off-the-shelf, bioactive scaffold that directs patient’s cells to align and differentiate into muscle tissue in situ. In this thesis, we developed fibrin microthreads, scaffolds composed of aligned fibrin material that direct cell alignment along the longitudinal axis of the microthread structure, with specific structural and biochemical properties to recreate structural cues lost in VML injuries. We hypothesized that fibrin microthreads with an increased resistance to proteolytic degradation and loaded with HGF would enhance the functional, mechanical regeneration of skeletal muscle tissue in a VML injury. We developed a crosslinking strategy to increase fibrin microthread resistance to enzymatic degradation, and increased their tensile strength and stiffness two- to three-fold. This crosslinking strategy enhanced the adsorption of HGF, facilitated its rapid release from microthreads for 2 to 3 days, and increased the chemotactic response of myoblasts twofold in 2D and 3D assays. Finally, we implanted HGF-loaded, crosslinked (EDCn-HGF) microthreads into a mouse model of VML to evaluate tissue regeneration and functional recovery. Fourteen days post-injury, we observed more muscle ingrowth along EDCn-HGF microthreads than untreated controls, suggesting that released HGF recruited additional progenitor cells to the injury site. Sixty days post-injury, EDCn-HGF microthreads guided mature, organized muscle to replace the microthreads in the wound site. Further, EDCn-HGF microthreads restored the contractile mechanical strength of the tissue to pre-injured values. In summary, we designed fibrin microthreads that recapitulate regenerative cues lost in VML injuries and enhance the functional regeneration of skeletal muscle.
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Books on the topic "Muscle regeneration"

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Stefano, Schiaffino, and Partridge Terence, eds. Skeletal muscle repair and regeneration. Dordrecht: Springer, 2008.

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Kyba, Michael, ed. Skeletal Muscle Regeneration in the Mouse. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3810-0.

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DeStefano, Rob. Muscle medicine: The revolutionary approach to maintaining, strengthening, and repairing your muscles and joints. New York: Fireside, 2009.

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4

B, Christ, Čihák Radomír, and European Anatomical Congress (7th : 1984 : Innsbruck, Austria), eds. Development and regeneration of skeletal muscles: Symposium held on occasion of the 7th European Anatomical Congress in Innsbruck, September 3, 1984. Basel: Karger, 1986.

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1895-1964, Blatz William Emet, and Kilborn Leslie G. 1895-1967, eds. Studies in the regeneration of denervated mammaliam muscle. Ottawa: J. de L. Taché, 1994.

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1935-, Oberpriller John O., Oberpriller Jean C. 1942-, Mauro Alexander, Rockefeller University, Cornell University Medical College, and Rosenfeld Heart Foundation, eds. The Development and regenerative potential of cardiac muscle. Chur: Harwood Academic Publishers, 1991.

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C, Claycomb William, Di Nardo Paolo, and New York Academy of Sciences., eds. Cardiac growth and regeneration. New York, N.Y: New York Academy of Sciences, 1995.

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White, Jason, and Gayle Smythe, eds. Growth Factors and Cytokines in Skeletal Muscle Development, Growth, Regeneration and Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27511-6.

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1953-, Angelov D. N., ed. Axonal branching and recovery of coordinated muscle activity after transection of the facial nerve in adult rats. Berlin: Springer, 2005.

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Coulthard, Rosalind Jane. The roles of motoneurons and their muscle targets in synaptogenesis during regeneration of a foreign transplant. Ottawa: National Library of Canada, 1998.

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Book chapters on the topic "Muscle regeneration"

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Canale, Enrico D., Gordon R. Campbell, Joseph J. Smolich, and Julie H. Campbell. "Regeneration." In Cardiac Muscle, 194. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-50115-9_9.

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Schmalbruch, H. "Development, Regeneration, Growth." In Skeletal Muscle, 239–303. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_7.

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Sevivas, Nuno, Guilherme França, Nuno Oliveira, Hélder Pereira, K. W. Ng, António Salgado, and João Espregueira-Mendes. "Biomaterials for Tendon Regeneration." In Muscle and Tendon Injuries, 131–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54184-5_13.

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Mittlmeier, Thomas, and Ioannis Stratos. "Muscle and Ligament Regeneration." In Regenerative Medicine, 921–34. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9075-1_38.

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Mittlmeier, Thomas, and Ioannis Stratos. "Muscle and Ligament Regeneration." In Regenerative Medicine, 1101–15. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-5690-8_42.

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Kim, Johnny, and Thomas Braun. "Skeletal Muscle Stem Cells for Muscle Regeneration." In Methods in Molecular Biology, 245–53. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1453-1_20.

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Ambrosio, Fabrisia, Yong Li, Arvydas Usas, Michael Boninger L., and Johnny Huard. "Muscle Repair after Injury and Disease." In Musculoskeletal Tissue Regeneration, 459–80. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-239-7_22.

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Cugat, R., E. Alentorn-Geli, J. M. Boffa, X. Cuscó, M. Garcia-Balletbo, P. Laiz, E. Mauri, and M. Rius. "Growth Factor Therapy for Tendon Regeneration." In Muscle and Tendon Injuries, 119–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54184-5_12.

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Stratos, Ioannis, and Thomas Mittlmeier. "Muscle, Ligament and Tendon Regeneration." In Regenerative Medicine - from Protocol to Patient, 349–66. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28386-9_11.

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Pipalia, Tapan G., Sami H. A. Sultan, Jana Koth, Robert D. Knight, and Simon M. Hughes. "Skeletal Muscle Regeneration in Zebrafish." In Methods in Molecular Biology, 227–48. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3036-5_17.

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Conference papers on the topic "Muscle regeneration"

1

Huang, Ping, Timon Cheng-Yi Liu, Xiao-Yang Xu, Xiao-Ying Chen, Jing Huang, Xiu-Feng Zhao, and Hong-Ying Pan. "Photobiomodulation on Muscle Regeneration." In 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4381920.

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Wulan, S. M. Mei. "Increasing Muscle Regeneration in Response to Exercise." In International Meeting on Regenerative Medicine. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007316000760080.

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Soker, Shay, Dawn Delo, Samira Neshat, and Anthony Atala. "Amniotic Fluid Derived Stem Cells for Cardiac Muscle Therapies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192492.

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Many forms of pediatric and adult heart disease are accompanied by high morbidity and mortality, as the heart muscle has limited regenerative potential. Cell therapy has been proposed as a means to promote the regeneration of injured heart muscle. We have established lines of broad spectrum multipotent stem cells derived from primitive fetal cells present in human amniotic fluid (hAFS) cells (1). AFS cells offer several advantages: They are easy to isolate and grow (no feeder layers needed), are highly expansive including clonal growth and they can differentiate into all germ layers. In the current study, we demonstrate that AFS cells can differentiate into cardiac muscle cells and be used for cardiac tissue regeneration.
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McKeon-Fischer, K. D., D. H. Flagg, J. H. Rossmeisl, A. R. Whittington, and J. W. Freeman. "Electroactive, Multi-Component Scaffolds for Skeletal Muscle Regeneration." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93197.

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After loss of skeletal muscle function due to traumatic injuries, muscle healing may result in scar tissue formation and reduced function. A restoration method is needed to create a bioartificial muscle that supports cell growth. An electroactive, coaxial electrospun scaffold was created using PCL, MWCNT, and a PAA/PVA hydrogel. This scaffold was conductive and displayed an actuation response when electrically stimulated. Rat primary skeletal muscle cells were biocompatible with the scaffold and displayed multi-nucleated constructs with actin interaction. MWCNT toxicity was tested using a single exposure method on rat primary skeletal muscle cells. A decrease in cellular activity was found on day 14, but a recovering trend was observed on days 21 and 28. Scaffolds were implanted in the quadriceps muscle of rats for in vivo biocompatibility investigation. Muscle cells were found to have attached and infiltrated the PCL-MWCNT-PAA/PVA scaffolds over the 28 day period. Further development of this scaffold would lead to a viable option for a bioartificial muscle as it is biocompatible and may provide some functional movement to the patient.
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Spadaccio, Cristiano, Alberto Rainer, Stefano De Porcellinis, Federico De Marco, Massimo Chello, Marcella Trombetta, and Jorge A. Genovese. "Muscle Reconstruction and Regeneration Using Biodegradable Scaffolds." In 2010 Advanced Technologies for Enhancing Quality of Life (ATEQUAL). IEEE, 2010. http://dx.doi.org/10.1109/atequal.2010.19.

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Cheesbrough, Aimee, Ivo Lieberam, and Wenhui Son. "Biobased Elastomer Nanofibers for Guiding Skeletal Muscle Regeneration." In The 7th World Congress on Recent Advances in Nanotechnology. Avestia Publishing, 2022. http://dx.doi.org/10.11159/nddte22.134.

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Errico, V., R. Molinaro, C. Gargioli, F. Ferranti, M. Dinescu, S. Cannata, G. Saggio, S. Rufini, and A. Desideri. "Cells Microenvironment Engineering - Multiphoton Absorption for Muscle Regeneration Optimization." In 9th International Conference on Biomedical Electronics and Devices. SCITEPRESS - Science and and Technology Publications, 2016. http://dx.doi.org/10.5220/0005790402410246.

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Cassino, Theresa R., Masaho Okada, Lauren M. Drowley, Joseph Feduska, Johnny Huard, and Philip R. LeDuc. "Using Mechanical Environment to Enhance Stem Cell Transplantation in Muscle Regeneration." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176545.

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Muscle-derived stem cell (MDSC) transplantation has shown potential as a therapy for cardiac and skeletal muscle dysfunction in diseases such as Duchenne muscular dystrophy (DMD). In this study we explore mechanical environment and its effects on MDSCs engraftment into cardiac and skeletal muscle in mdx mice and neoangiogenesis within the engraftment area. We first looked at transplantation of the same number of MDSCs into the heart and gastrocnemius (GN) muscle of dystrophic mice and the resulting dystrophin expression. We then explored neoangiogenesis within the engraftments through quantification of CD31 positive microvessels. This study is important to aid in determining the in vivo environmental factors leading to large graft size which may aid in determining optimum transplantation conditions for muscle repair.
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Willett, Nick J., M. Alice Li, Brent A. Uhrig, Gordon L. Warren, and Robert E. Guldberg. "Muscle Injury Attenuates BMP-2 Mediated Tissue Regeneration in a Novel Rat Model of Composite Bone and Muscle Injury." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53589.

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Musculoskeletal diseases and injuries are a major burden on society, representing the most common cause of pain and impaired function worldwide. Composite injuries involving bone and the surrounding soft tissue comprise one of the most challenging musculoskeletal conditions to return to normal function. During repair of these injuries there is a loss of the synergistic interactions between adjacent tissues resulting in impaired bone regeneration. Additionally, local soft tissue ischemia may also be a contributing factor to increased infection rates observed in severe composite tissue injuries. Muscle has been implicated as a source for re-vascularization, osteoprogenitor cells and osteogenic factors, as well as a contributor to the biomechanical stimuli; however, associated studies have mostly been qualitative in nature, offering little insight into the mechanistic nature of the relationship of soft tissue to bone regeneration. Small animal models of critically sized bone defects are an efficient means to test engraftment strategies of novel constructs and therapeutics particularly in terms of functional restoration of a limb. Our lab previously developed a critically-sized rat segmental defect model with which we have quantitatively assessed bone regeneration using numerous constructs and therapeutic treatments [1]. Our objective was to develop a composite injury model by combining this segmental defect model with a muscle injury adjacent to the bone defect. We hypothesized that animals with a composite injury would have attenuated BMP-2 mediated tissue regeneration as compared to animals with a single tissue injury.
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Calve, Sarah, and Hans-Georg Simon. "The Mechanical and Biochemical Environment Controls Cellular Differentiation During Muscle Regeneration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53767.

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Urodele amphibians like the newt, are able to completely regenerate lost organs and appendages without scarring. Differentiated tissues are considered a reservoir for uncommitted blastema cells that participate in the regeneration of the lost structure. To determine the influence of the extracellular matrix (ECM) on the recruitment of progenitor cells from the skeletal muscle, we immunohistochemically mapped the limb in 3D and found that a transitional ECM rich in hyaluronic acid (HA), tenascin-C (TN) and fibronectin (FN) is dynamically expressed during the early stages of regeneration [1]. Functional in vitro testing of different ECM components on primary muscle cells revealed that HA and TN support myoblast migration, inhibit differentiation and enhance the fragmentation of multinucleate myotubes and production of viable mononucleate myoblasts, cellular behaviors necessary for blastema formation [1]. In contrast, myoblasts plated on matrices that mimic ECM around differentiated muscle (FN, Matrigel and laminin) induced both proliferation and fusion.
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Reports on the topic "Muscle regeneration"

1

Gonzalez-Cadavid, Nestor F. Modulation of Stem Cell Differentiation and Myostatin as an Approach to Counteract Fibrosis in Muscle Dystrophy and Regeneration After Injury. Addendum. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada586854.

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Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.sup.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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