Journal articles on the topic 'Skeletal muscle satellite cells'
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Yablonka-Reuveni, Zipora. "The Skeletal Muscle Satellite Cell." Journal of Histochemistry & Cytochemistry 59, no. 12 (December 2011): 1041–59. http://dx.doi.org/10.1369/0022155411426780.
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The skeletal muscle satellite cell was first described and named based on its anatomic location between the myofiber plasma and basement membranes. In 1961, two independent studies by Alexander Mauro and Bernard Katz provided the first electron microscopic descriptions of satellite cells in frog and rat muscles. These cells were soon detected in other vertebrates and acquired candidacy as the source of myogenic cells needed for myofiber growth and repair throughout life. Cultures of isolated myofibers and, subsequently, transplantation of single myofibers demonstrated that satellite cells were myogenic progenitors. More recently, satellite cells were redefined as myogenic stem cells given their ability to self-renew in addition to producing differentiated progeny. Identification of distinctively expressed molecular markers, in particular Pax7, has facilitated detection of satellite cells using light microscopy. Notwithstanding the remarkable progress made since the discovery of satellite cells, researchers have looked for alternative cells with myogenic capacity that can potentially be used for whole body cell-based therapy of skeletal muscle. Yet, new studies show that inducible ablation of satellite cells in adult muscle impairs myofiber regeneration. Thus, on the 50th anniversary since its discovery, the satellite cell’s indispensable role in muscle repair has been reaffirmed.
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Azab, Azab. "Skeletal Muscles: Insight into Embryonic Development, Satellite Cells, Histology, Ultrastructure, Innervation, Contraction and Relaxation, Causes, Pathophysiology, and Treatment of Volumetric Muscle I." Biotechnology and Bioprocessing 2, no. 4 (May 28, 2021): 01–17. http://dx.doi.org/10.31579/2766-2314/038.
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Background: Skeletal muscles are attached to bone and are responsible for the axial and appendicular movement of the skeleton and for maintenance of body position and posture. Objectives: The present review aimed to high light on embryonic development of skeletal muscles, histological and ultrastructure, innervation, contraction and relaxation, causes, pathophysiology, and treatment of volumetric muscle injury. The heterogeneity of the muscle fibers is the base of the flexibility which allows the same muscle to be used for various tasks from continuous low-intensity activity, to repeated submaximal contractions, and to fast and strong maximal contractions. The formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts. As growth of the muscle fibers continues, aggregation into bundles occurs, and by birth, myoblast activity has ceased. Satellite cells (SCs), have single nuclei and act as regenerative cells. Satellite cells are the resident stem cells of skeletal muscle; they are considered to be self-renewing and serve to generate a population of differentiation-competent myoblasts that will participate as needed in muscle growth, repair, and regeneration. Based on various structural and functional characteristics, skeletal muscle fibres are classified into three types: Type I fibres, Type II-B fibres, and type II-A fibres. Skeletal muscle fibres vary in colour depending on their content of myoglobin. Each myofibril exhibits a repeating pattern of cross-striations which is a product of the highly ordered arrangement of the contractile proteins within it. The parallel myofibrils are arranged with their cross-striations in the register, giving rise to the regular striations seen with light microscopy in longitudinal sections of skeletal muscle. Each skeletal muscle receives at least two types of nerve fibers: motor and sensory. Striated muscles and myotendinous junctions contain sensory receptors that are encapsulated proprioceptors. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. During muscle contraction, the thin filaments slide past the thick filaments, as proposed by Huxley's sliding filament theory. In response to a muscle injury, SCs are activated and start to proliferate; at this stage, they are often referred to as either myogenic precursor cells (MPC) or myoblasts. In vitro, evidence has been presented that satellite cells can be pushed towards the adipogenic and osteogenic lineages, but contamination of such cultures from non-myogenic cells is sometimes hard to dismiss as the underlying cause of this observed multipotency. There are, however, other populations of progenitors isolated from skeletal muscle, including endothelial cells and muscle-derived stem cells (MDSCs), blood-vessel-associated mesoangioblasts, muscle side-population cells, CD133+ve cells, myoendothelial cells, and pericytes. Volumetric muscle loss (VML) is defined as the traumatic or surgical loss of skeletal muscle with resultant functional impairment. It represents a challenging clinical problem for both military and civilian medicine. VML results in severe cosmetic deformities and debilitating functional loss. In response to damage, skeletal muscle goes through a well-defined series of events including; degeneration (1 to 3days), inflammation, and regeneration (3 to 4 weeks), fibrosis, and extracellular matrix remodeling (3 to 6 months).. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. During muscle tissue repair following damage, the degree of damage and the interactions between muscle and the infiltrating inflammatory cells appear to affect the successful outcome of the muscle repair process. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering. Conclusion: It can be concluded that the formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts, by birth myoblast activity has ceased. Satellite cells are considered to be self-renewing, and serve to generate a population of differentiation-competent myoblasts. Skeletal muscle fibres are classified into three types. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. VML results in severe cosmetic deformities and debilitating functional loss. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering.
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Shadrach, Jennifer L., and Amy J. Wagers. "Stem cells for skeletal muscle repair." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1575 (August 12, 2011): 2297–306. http://dx.doi.org/10.1098/rstb.2011.0027.
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Skeletal muscle is a highly specialized tissue composed of non-dividing, multi-nucleated muscle fibres that contract to generate force in a controlled and directed manner. Skeletal muscle is formed during embryogenesis from a subset of muscle precursor cells, which generate both differentiated muscle fibres and specialized muscle-forming stem cells known as satellite cells. Satellite cells remain associated with muscle fibres after birth and are responsible for muscle growth and repair throughout life. Failure in satellite cell function can lead to delayed, impaired or failed recovery after muscle injury, and such failures become increasingly prominent in cases of progressive muscle disease and in old age. Recent progress in the isolation of muscle satellite cells and elucidation of the cellular and molecular mediators controlling their activity indicate that these cells represent promising therapeutic targets. Such satellite cell-based therapies may involve either direct cell replacement or development of drugs that enhance endogenous muscle repair mechanisms. Here, we discuss recent breakthroughs in understanding both the cell intrinsic and extrinsic regulators that determine the formation and function of muscle satellite cells, as well as promising paths forward to realizing their full therapeutic potential.
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Eržen, Ida. "PLASTICITY OF SKELETAL MUSCLE STUDIED BY STEREOLOGY." Image Analysis & Stereology 23, no. 3 (May 3, 2011): 143. http://dx.doi.org/10.5566/ias.v23.p143-152.
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The present contribution provides an overview of stereological methods applied in the skeletal muscle research at the Institute of Anatomy of the Medical Faculty in Ljubljana. Interested in skeletal muscle plasticity we studied three different topics: (i) expression of myosin heavy chain isoforms in slow and fast muscles under experimental conditions, (ii) frequency of satellite cells in young and old human and rat muscles and (iii) capillary supply of rat fast and slow muscles. We analysed the expression of myosin heavy chain isoforms within slow rat soleus and fast extensor digitorum longus muscles after (i) homotopic and heterotopic transplantation of both muscles, (ii) low frequency electrical stimulation of the fast muscle and (iii) transposition of the fast nerve to the slow muscle. The models applied were able to turn the fast muscle into a completely slow muscle, but not vice versa. One of the indicators for the regenerative potential of skeletal muscles is its satellite cell pool. The estimated parameters, number of satellite cells per unit fibre length, corrected to the reference sarcomere length (Nsc/Lfib) and number of satellite cells per number of nuclei (myonuclei and satellite cell nuclei) (Nsc/Nnucl) indicated that the frequency of M-cadherin stained satellite cells declines in healthy old human and rat muscles compared to young muscles. To access differences in capillary densities among slow and fast muscles and slow and fast muscle fibres, we have introduced Slicer and Fakir methods, and tested them on predominantly slow and fast rat muscles. Discussing three different topics that require different approach, the present paper reflects the three decades of the development of stereological methods: 2D analysis by simple point counting in the 70's, the disector in the 80's and virtual spatial probes in the 90's. In all methods the interactive computer assisted approach was utilised.
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CIECIERSKA, ANNA, TOMASZ SADKOWSKI, and TOMASZ MOTYL. "Role of satellite cells in growth and regeneration of skeletal muscles." Medycyna Weterynaryjna 75, no. 11 (2019): 6349–2019. http://dx.doi.org/10.21521/mw.6349.
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Postnatal growth and regeneration capacity of skeletal muscles is dependent mainly on adult muscle stem cells called satellite cells. Satellite cells are quiescent mononucleated cells that are normally located outside the sarcolemma within the basal lamina of the muscle fiber. Their activation, which results from injury, is manifested by mobilization, proliferation, differentiation and, ultimately, fusion into new muscle fibers. The satellite cell pool is responsible for the remarkable regenerative capacity of skeletal muscles. Moreover, these cells are capable of self-renewal and can give rise to myogenic progeny.
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Bischoff, Richard. "Chemotaxis of skeletal muscle satellite cells." Developmental Dynamics 208, no. 4 (April 1997): 505–15. http://dx.doi.org/10.1002/(sici)1097-0177(199704)208:4<505::aid-aja6>3.0.co;2-m.
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Jurdana, Mihaela. "EXERCISE EFFECTS ON MUSCLE STEM CELLS." Annales Kinesiologiae 8, no. 2 (January 26, 2018): 125–35. http://dx.doi.org/10.35469/ak.2017.134.
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Satellite cells are skeletal muscle stem cells that facilitate muscle repair and regeneration after “damage” which occurs after physiological stimuli: exercise, post-training micro-injuries and electrical stimulation. Exercise stimuli lead to activation and proliferation of these cells from their quiescent state, therefore, increasing cell numbers having the potential to provide additional myonuclei to their parent muscle fibre or return to a quiescent state. Different exercise modalities are the focus of numerous studies on satellite cells activation. An increase in muscle activity augments satellite cells proliferation as well as skeletal muscle mass and function, both in young and elderly.
This review provides an updated view of the contribution of skeletal muscle satellite cells in regulating skeletal muscle mass and the efficiency of the exercise intervention to attenuate the decline in muscle mass.
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Yin, Hang, Feodor Price, and Michael A. Rudnicki. "Satellite Cells and the Muscle Stem Cell Niche." Physiological Reviews 93, no. 1 (January 2013): 23–67. http://dx.doi.org/10.1152/physrev.00043.2011.
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Adult skeletal muscle in mammals is a stable tissue under normal circumstances but has remarkable ability to repair after injury. Skeletal muscle regeneration is a highly orchestrated process involving the activation of various cellular and molecular responses. As skeletal muscle stem cells, satellite cells play an indispensible role in this process. The self-renewing proliferation of satellite cells not only maintains the stem cell population but also provides numerous myogenic cells, which proliferate, differentiate, fuse, and lead to new myofiber formation and reconstitution of a functional contractile apparatus. The complex behavior of satellite cells during skeletal muscle regeneration is tightly regulated through the dynamic interplay between intrinsic factors within satellite cells and extrinsic factors constituting the muscle stem cell niche/microenvironment. For the last half century, the advance of molecular biology, cell biology, and genetics has greatly improved our understanding of skeletal muscle biology. Here, we review some recent advances, with focuses on functions of satellite cells and their niche during the process of skeletal muscle regeneration.
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Englund, Davis A., Bailey D. Peck, Kevin A. Murach, Ally C. Neal, Hannah A. Caldwell, John J. McCarthy, Charlotte A. Peterson, and Esther E. Dupont-Versteegden. "Resident muscle stem cells are not required for testosterone-induced skeletal muscle hypertrophy." American Journal of Physiology-Cell Physiology 317, no. 4 (October 1, 2019): C719—C724. http://dx.doi.org/10.1152/ajpcell.00260.2019.
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It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this hypothesis, we utilized the Pax7-DTA mouse model to deplete satellite cells in skeletal muscle followed by testosterone administration. Pax7-DTA mice (6 mo of age) were treated for 5 days with either vehicle [satellite cell replete (SC+)] or tamoxifen [satellite cell depleted (SC-)]. Following a washout period, a testosterone propionate or sham pellet was implanted for 21 days. Testosterone administration caused a significant increase in muscle fiber cross-sectional area in SC+ and SC- mice in both oxidative (soleus) and glycolytic (plantaris and extensor digitorum longus) muscles. In SC+ mice treated with testosterone, there was a significant increase in both satellite cell abundance and myonuclei that was completely absent in testosterone-treated SC- mice. These findings provide direct evidence that testosterone-induced muscle fiber hypertrophy does not require an increase in satellite cell abundance or myonuclear accretion. Listen to a podcast about this Rapid Report with senior author E. E. Dupont-Versteegden ( https://ajpcell.podbean.com/e/podcast-on-paper-that-shows-testosterone-induced-skeletal-muscle-hypertrophy-does-not-need-muscle-stem-cells /).
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Adams, Gregory R. "Satellite cell proliferation and skeletal muscle hypertrophy." Applied Physiology, Nutrition, and Metabolism 31, no. 6 (December 2006): 782–90. http://dx.doi.org/10.1139/h06-053.
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Satellite cells are small, mononuclear cells found in close association with striated skeletal muscles cells (myofibers). These cells appear to function as reserve myoblasts. A critical role for these cells in the process of muscle regeneration following injury has been clearly established. In that role, satellite cells have been shown to proliferate extensively. Some of the progeny of these cells then fuse with each other to form replacement myofibers, whereas others return to quiescence, thereby maintaining this reserve population. In response to injury, activated satellite cells can also fuse with damaged but viable myofibers to promote repair and regeneration. It has also been observed that satellite cells are activated during periods of significantly increased muscle loading and that some of these cells fuse with apparently undamaged myofibers as part of the hypertrophy process. The observation that the inactivation of satellite cell proliferation prevents most of the hypertrophy response to chronic increases in loading has lead to the hypothesis that a limitation to the expansion of myofiber size is imposed by the number of myonuclei present. Recent evidence suggests that a potential limitation to muscle hypertrophy, in the absence of a reserve supply of myonuclei, may be the inability to sustain increases in ribosomes, thereby limiting translational capacity.
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Wang, Shaoyu, Kui Li, Hui Gao, Zepeng Liu, Shuang Shi, Qiang Tan, and Zhengguang Wang. "Ubiquitin-specific peptidase 8 regulates proliferation and early differentiation of sheep skeletal muscle satellite cells." Czech Journal of Animal Science 66, No. 3 (March 2, 2021): 87–96. http://dx.doi.org/10.17221/105/2020-cjas.
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Ubiquitin-specific protease 8 (USP8), a member of the ubiquitin-specific protease (USP) family, was originally identified as playing a role in the regulation of growth and cell cycle. However, its functional role in myogenesis is unknown. In this study, we investigated the role of USP8 in proliferation and differentiation of sheep skeletal muscle satellite cells. The results showed that the expression level of USP8 was significantly increased on days 2 and 3 following the induction of the differentiation process. Furthermore, knocking down USP8 resulted in a significant increase in myogenin-positive cells, and promoted early differentiation of satellite cells by regulating the expression level of paired box 7 (PAX7). Additionally, knocking down USP8 suppressed muscle satellite cell proliferation, possibly explaining that the relative mRNA level of USP8 was linearly related to muscle fibre density of Hu sheep. Overall, our research demonstrates that USP8 plays a role in proliferation and early differentiation of skeletal muscle satellite cells.
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Englund, Davis A., Kevin A. Murach, Cory M. Dungan, Vandré C. Figueiredo, Ivan J. Vechetti, Esther E. Dupont-Versteegden, John J. McCarthy, and Charlotte A. Peterson. "Depletion of resident muscle stem cells negatively impacts running volume, physical function, and muscle fiber hypertrophy in response to lifelong physical activity." American Journal of Physiology-Cell Physiology 318, no. 6 (June 1, 2020): C1178—C1188. http://dx.doi.org/10.1152/ajpcell.00090.2020.
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To date, studies that have aimed to investigate the role of satellite cells during adult skeletal muscle adaptation and hypertrophy have utilized a nontranslational stimulus and/or have been performed over a relatively short time frame. Although it has been shown that satellite cell depletion throughout adulthood does not drive skeletal muscle loss in sedentary mice, it remains unknown how satellite cells participate in skeletal muscle adaptation to long-term physical activity. The current study was designed to determine whether reduced satellite cell content throughout adulthood would influence the transcriptome-wide response to physical activity and diminish the adaptive response of skeletal muscle. We administered vehicle or tamoxifen to adult Pax7-diphtheria toxin A (DTA) mice to deplete satellite cells and assigned them to sedentary or wheel-running conditions for 13 mo. Satellite cell depletion throughout adulthood reduced balance and coordination, overall running volume, and the size of muscle proprioceptors (spindle fibers). Furthermore, satellite cell participation was necessary for optimal muscle fiber hypertrophy but not adaptations in fiber type distribution in response to lifelong physical activity. Transcriptome-wide analysis of the plantaris and soleus revealed that satellite cell function is muscle type specific; satellite cell-dependent myonuclear accretion was apparent in oxidative muscles, whereas initiation of G protein-coupled receptor (GPCR) signaling in the glycolytic plantaris may require satellite cells to induce optimal adaptations to long-term physical activity. These findings suggest that satellite cells play a role in preserving physical function during aging and influence muscle adaptation during sustained periods of physical activity.
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De Angelis, Luciana, Libera Berghella, Marcello Coletta, Laura Lattanzi, Malvina Zanchi, M. Gabriella, Carola Ponzetto, and Giulio Cossu. "Skeletal Myogenic Progenitors Originating from Embryonic Dorsal Aorta Coexpress Endothelial and Myogenic Markers and Contribute to Postnatal Muscle Growth and Regeneration." Journal of Cell Biology 147, no. 4 (November 15, 1999): 869–78. http://dx.doi.org/10.1083/jcb.147.4.869.
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Skeletal muscle in vertebrates is derived from somites, epithelial structures of the paraxial mesoderm, yet many unrelated reports describe the occasional appearance of myogenic cells from tissues of nonsomite origin, suggesting either transdifferentiation or the persistence of a multipotent progenitor. Here, we show that clonable skeletal myogenic cells are present in the embryonic dorsal aorta of mouse embryos. This finding is based on a detailed clonal analysis of different tissue anlagen at various developmental stages. In vitro, these myogenic cells show the same morphology as satellite cells derived from adult skeletal muscle, and express a number of myogenic and endothelial markers. Surprisingly, the latter are also expressed by adult satellite cells. Furthermore, it is possible to clone myogenic cells from limbs of mutant c-Met−/− embryos, which lack appendicular muscles, but have a normal vascular system. Upon transplantation, aorta-derived myogenic cells participate in postnatal muscle growth and regeneration, and fuse with resident satellite cells. The potential of the vascular system to generate skeletal muscle cells may explain observations of nonsomite skeletal myogenesis and raises the possibility that a subset of satellite cells may derive from the vascular system.
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Alfaqih, Muhammad Subhan, Vita Murniati Tarawan, Nova Sylviana, Hanna Goenawan, Ronny Lesmana, and Susianti Susianti. "Effects of Vitamin D on Satellite Cells: A Systematic Review of In Vivo Studies." Nutrients 14, no. 21 (October 29, 2022): 4558. http://dx.doi.org/10.3390/nu14214558.
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The non-classical role of vitamin D has been investigated in recent decades. One of which is related to its role in skeletal muscle. Satellite cells are skeletal muscle stem cells that play a pivotal role in skeletal muscle growth and regeneration. This systematic review aims to investigate the effect of vitamin D on satellite cells. A systematic search was performed in Scopus, MEDLINE, and Google Scholar. In vivo studies assessing the effect of vitamin D on satellite cells, published in English in the last ten years were included. Thirteen in vivo studies were analyzed in this review. Vitamin D increases the proliferation of satellite cells in the early life period. In acute muscle injury, vitamin D deficiency reduces satellite cells differentiation. However, administering high doses of vitamin D impairs skeletal muscle regeneration. Vitamin D may maintain satellite cell quiescence and prevent spontaneous differentiation in aging. Supplementation of vitamin D ameliorates decreased satellite cells’ function in chronic disease. Overall, evidence suggests that vitamin D affects satellite cells’ function in maintaining skeletal muscle homeostasis. Further research is needed to determine the most appropriate dose of vitamin D supplementation in a specific condition for the optimum satellite cells’ function.
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Forcina, Laura, Carmen Miano, Laura Pelosi, and Antonio Musarò. "An Overview About the Biology of Skeletal Muscle Satellite Cells." Current Genomics 20, no. 1 (February 27, 2019): 24–37. http://dx.doi.org/10.2174/1389202920666190116094736.
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The peculiar ability of skeletal muscle tissue to operate adaptive changes during post-natal development and adulthood has been associated with the existence of adult somatic stem cells. Satellite cells, occupying an exclusive niche within the adult muscle tissue, are considered bona fide stem cells with both stem-like properties and myogenic activities. Indeed, satellite cells retain the capability to both maintain the quiescence in uninjured muscles and to be promptly activated in response to growth or regenerative signals, re-engaging the cell cycle. Activated cells can undergo myogenic differentiation or self-renewal moving back to the quiescent state. Satellite cells behavior and their fate decision are finely controlled by mechanisms involving both cell-autonomous and external stimuli. Alterations in these regulatory networks profoundly affect muscle homeostasis and the dynamic response to tissue damage, contributing to the decline of skeletal muscle that occurs under physio-pathologic conditions. Although the clear myogenic activity of satellite cells has been described and their pivotal role in muscle growth and regeneration has been reported, a comprehensive picture of inter-related mechanisms guiding muscle stem cell activity has still to be defined. Here, we reviewed the main regulatory networks determining satellite cell behavior. In particular, we focused on genetic and epigenetic mechanisms underlining satellite cell maintenance and commitment. Besides intrinsic regulations, we reported current evidences about the influence of environmental stimuli, derived from other cell populations within muscle tissue, on satellite cell biology.
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Yoshioka, Kiyoshi, Hiroshi Nagahisa, Fumihito Miura, Hiromitsu Araki, Yasutomi Kamei, Yasuo Kitajima, Daiki Seko, et al. "Hoxa10 mediates positional memory to govern stem cell function in adult skeletal muscle." Science Advances 7, no. 24 (June 2021): eabd7924. http://dx.doi.org/10.1126/sciadv.abd7924.
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Muscle stem cells (satellite cells) are distributed throughout the body and have heterogeneous properties among muscles. However, functional topographical genes in satellite cells of adult muscle remain unidentified. Here, we show that expression of Homeobox-A (Hox-A) cluster genes accompanied with DNA hypermethylation of the Hox-A locus was robustly maintained in both somite-derived muscles and their associated satellite cells in adult mice, which recapitulates their embryonic origin. Somite-derived satellite cells were clearly separated from cells derived from cranial mesoderm in Hoxa10 expression. Hoxa10 inactivation led to genomic instability and mitotic catastrophe in somite-derived satellite cells in mice and human. Satellite cell–specific Hoxa10 ablation in mice resulted in a decline in the regenerative ability of somite-derived muscles, which were unobserved in cranial mesoderm–derived muscles. Thus, our results show that Hox gene expression profiles instill the embryonic history in satellite cells as positional memory, potentially modulating region-specific pathophysiology in adult muscles.
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Stern-Straeter, Jens, Juritz Stephanie, Gregor Bran, Frank Riedel, Haneen Sadick, Karl Hörmann, and Ulrich R. Goessler. "Skeletal Muscle Regeneration: MSC versus Satellite Cells." Otolaryngology–Head and Neck Surgery 139, no. 2_suppl (August 2008): P86. http://dx.doi.org/10.1016/j.otohns.2008.05.484.
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Problem Differentiating stem cells into the myogenic linage in order to create functional muscle tissue is a challenging endeavour. In this work, adipose-derived mesenchymal stem cells (MSC) and satellite cells derived from muscle biopsies were compared regarding proliferation and myogenic differentiation potential under standardized cell culture conditions. This data was obtained in order to discover the most promising type of stem cell for regeneration of muscle tissue and to determine the optimal culture conditions for later clinical use. Methods Human MSC were isolated from adipose tissue, and primary human skeletal myoblasts were extracted from muscle biopsies by enzymatic digestion. Proliferation was analysed using the AlamarBlue® assay. Gene expression of marker genes – such as Myogenin, Myo D, Myf 5 and MHC – were analysed by RT-PCR. Immunostainings against desmin and sarcomeric-actin were performed as differentiation markers. Results MSC cell cultures showed a greater proliferation rate compared with satellite cell cultures. In both stem cell cultures, myogenic differentiation/heritage could be verified by immunostainings against the muscle-specific marker desmin. Gene expression and protein analysis revealed a more stable differentiation of human satellite cell cultures. Conclusion Characterization of both human MSC cultures and satellite cell cultures – and thereby an understanding of myogenesis – might lead to their clinical usage in skeletal muscle tissue engineering. The results in this study appear to indicate that human satellite cell cultures have a more stable differentiation under in vitro conditions and that they might offer a greater potential for skeletal muscle tissue engineering purposes. Significance Our study contributes to the understanding of myogenic differentiation of MSC and satellite cells and helps to improve culture systems for later clinical utilization.
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Zhang, Zihao, Shudai Lin, Wen Luo, Tuanhui Ren, Xing Huang, Wangyu Li, and Xiquan Zhang. "Sox6 Differentially Regulates Inherited Myogenic Abilities and Muscle Fiber Types of Satellite Cells Derived from Fast- and Slow-Type Muscles." International Journal of Molecular Sciences 23, no. 19 (September 26, 2022): 11327. http://dx.doi.org/10.3390/ijms231911327.
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Adult skeletal muscle is primarily divided into fast and slow-type muscles, which have distinct capacities for regeneration, metabolism and contractibility. Satellite cells plays an important role in adult skeletal muscle. However, the underlying mechanisms of satellite cell myogenesis are poorly understood. We previously found that Sox6 was highly expressed in adult fast-type muscle. Therefore, we aimed to validate the satellite cell myogenesis from different muscle fiber types and investigate the regulation of Sox6 on satellite cell myogenesis. First, we isolated satellite cells from fast- and slow-type muscles individually. We found that satellite cells derived from different muscle fiber types generated myotubes similar to their origin types. Further, we observed that cells derived from fast muscles had a higher efficiency to proliferate but lower potential to self-renew compared to the cells derived from slow muscles. Then we demonstrated that Sox6 facilitated the development of satellite cells-derived myotubes toward their inherent muscle fiber types. We revealed that higher expression of Nfix during the differentiation of fast-type muscle-derived myogenic cells inhibited the transcription of slow-type isoforms (MyH7B, Tnnc1) by binding to Sox6. On the other hand, Sox6 activated Mef2C to promote the slow fiber formation in slow-type muscle-derived myogenic cells with Nfix low expression, showing a different effect of Sox6 on the regulation of satellite cell development. Our findings demonstrated that satellite cells, the myogenic progenitor cells, tend to develop towards the fiber type similar to where they originated. The expression of Sox6 and Nfix partially explain the developmental differences of myogenic cells derived from fast- and slow-type muscles.
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Yoshimoto, Momoko, Toshio Heike, Mitsutaka Shiota, Hirohiko Kobayashi, Katsutsugu Umeda, and Tatsutoshi Nakahata. "Hematopoietic Stem Cells Can Give Rise to Satellite-Like Cells in Skeletal Muscles." Blood 104, no. 11 (November 16, 2004): 2690. http://dx.doi.org/10.1182/blood.v104.11.2690.2690.
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Abstract Recent studies have indicated that bone marrow cells can regenerate damaged muscles, but also that they can adopt phenotype of other cells by cell fusion. It has also been reported that single hematopoietic stem cells (HSCs) can regenerate skeletal muscle although it is still controversial whether HSCs differentiate into satellite cells in muscle or not. In order to investigate the roles of HSCs in muscle regeneration and whether they can generate satellite cells or not, we purified and injected CD45+Lin−Sca-1+c-kit+(CD45+KSL) HSCs labeled by green fluorescent protein (GFP) into mice with or without irradiation. We examined time-course behavior of HSCs in recipient muscles with a fluorescent stereomicroscope and then immunohitochemical staining during the early and late phase after transplantation. Our direct visualization system gave evidence of massive GFP signals in all the muscles of only irradiated mice in early phase after transplantation. Transverse cryostat sections showed GFP+ Myosin+ muscle fibers along with numerous GFP+ hematopoietic cells in damaged muscle. We also found myogenin+GFP+ cells like myoblasts in very low number. These phenomena were temporal and GFP signals had dramatically reduced 30 days after transplantation. FISH analysis confirmed the GFP-DNAs in the nuclei of muscle fibers. These results suggested that most of GFP+HSCs fused with myofibers and participated in regeneration of damaged muscles, and a very few HSCs can differentiate into myoblast like cells expressing myogenin. After 6 months, GFP+ fibers could be hardly detected but GFP+c-Met+ mononuclear cells were located beneath the laminin+ basal lamina. Single fiber cultures from these mice showed proliferation of GFP+ fibers. These results suggested that HSC-derived cells settled beneath the basal lamina like satellite cells and might acquired the satellite cell activity.
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Sanna, Marta, Chiara Franzin, Michela Pozzobon, Francesca Favaretto, Carlo Alberto Rossi, Alessandra Calcagno, Alessandro Scarda, et al. "Adipogenic potential of skeletal muscle satellite cells." Clinical Lipidology 4, no. 2 (April 2009): 245–65. http://dx.doi.org/10.2217/clp.09.8.
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Criswell, David. "Redox Control of Skeletal Muscle Satellite Cells." Medicine & Science in Sports & Exercise 41 (May 2009): 17. http://dx.doi.org/10.1249/01.mss.0000352742.08641.78.
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Le Grand, Fabien, and Michael A. Rudnicki. "Skeletal muscle satellite cells and adult myogenesis." Current Opinion in Cell Biology 19, no. 6 (December 2007): 628–33. http://dx.doi.org/10.1016/j.ceb.2007.09.012.
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Asakura, Atsushi, Patrick Seale, Adele Girgis-Gabardo, and Michael A. Rudnicki. "Myogenic specification of side population cells in skeletal muscle." Journal of Cell Biology 159, no. 1 (October 14, 2002): 123–34. http://dx.doi.org/10.1083/jcb.200202092.
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Skeletal muscle contains myogenic progenitors called satellite cells and muscle-derived stem cells that have been suggested to be pluripotent. We further investigated the differentiation potential of muscle-derived stem cells and satellite cells to elucidate relationships between these two populations of cells. FACS® analysis of muscle side population (SP) cells, a fraction of muscle-derived stem cells, revealed expression of hematopoietic stem cell marker Sca-1 but did not reveal expression of any satellite cell markers. Muscle SP cells were greatly enriched for cells competent to form hematopoietic colonies. Moreover, muscle SP cells with hematopoietic potential were CD45 positive. However, muscle SP cells did not differentiate into myocytes in vitro. By contrast, satellite cells gave rise to myocytes but did not express Sca-1 or CD45 and never formed hematopoietic colonies. Importantly, muscle SP cells exhibited the potential to give rise to both myocytes and satellite cells after intramuscular transplantation. In addition, muscle SP cells underwent myogenic specification after co-culture with myoblasts. Co-culture with myoblasts or forced expression of MyoD also induced muscle differentiation of muscle SP cells prepared from mice lacking Pax7 gene, an essential gene for satellite cell development. Therefore, these data document that satellite cells and muscle-derived stem cells represent distinct populations and demonstrate that muscle-derived stem cells have the potential to give rise to myogenic cells via a myocyte-mediated inductive interaction.
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Straughn, Alex R., Sajedah M. Hindi, Guangyan Xiong, and Ashok Kumar. "Canonical NF-κB signaling regulates satellite stem cell homeostasis and function during regenerative myogenesis." Journal of Molecular Cell Biology 11, no. 1 (September 19, 2018): 53–66. http://dx.doi.org/10.1093/jmcb/mjy053.
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Abstract Skeletal muscle regeneration in adults is attributed to the presence of satellite stem cells that proliferate, differentiate, and eventually fuse with injured myofibers. However, the signaling mechanisms that regulate satellite cell homeostasis and function remain less understood. While IKKβ-mediated canonical NF-κB signaling has been implicated in the regulation of myogenesis and skeletal muscle mass, its role in the regulation of satellite cell function during muscle regeneration has not been fully elucidated. Here, we report that canonical NF-κB signaling is induced in skeletal muscle upon injury. Satellite cell-specific inducible ablation of IKKβ attenuates skeletal muscle regeneration in adult mice. Targeted ablation of IKKβ also reduces the number of satellite cells in injured skeletal muscle of adult mice, potentially through inhibiting their proliferation and survival. We also demonstrate that the inhibition of specific components of the canonical NF-κB pathway causes precocious differentiation of cultured satellite cells both ex vivo and in vitro. Finally, our results highlight that the constitutive activation of canonical NF-κB signaling in satellite cells also attenuates skeletal muscle regeneration following injury in adult mice. Collectively, our study demonstrates that the proper regulation of canonical NF-κB signaling is important for the regeneration of adult skeletal muscle.
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Roux-Biejat, Paulina, Marco Coazzoli, Pasquale Marrazzo, Silvia Zecchini, Ilaria Di Renzo, Cecilia Prata, Alessandra Napoli, et al. "Acid Sphingomyelinase Controls Early Phases of Skeletal Muscle Regeneration by Shaping the Macrophage Phenotype." Cells 10, no. 11 (November 5, 2021): 3028. http://dx.doi.org/10.3390/cells10113028.
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Skeletal muscle regeneration is a complex process involving crosstalk between immune cells and myogenic precursor cells, i.e., satellite cells. In this scenario, macrophage recruitment in damaged muscles is a mandatory step for tissue repair since pro-inflammatory M1 macrophages promote the activation of satellite cells, stimulating their proliferation and then, after switching into anti-inflammatory M2 macrophages, they prompt satellite cells’ differentiation into myotubes and resolve inflammation. Here, we show that acid sphingomyelinase (ASMase), a key enzyme in sphingolipid metabolism, is activated after skeletal muscle injury induced in vivo by the injection of cardiotoxin. ASMase ablation shortens the early phases of skeletal muscle regeneration without affecting satellite cell behavior. Of interest, ASMase regulates the balance between M1 and M2 macrophages in the injured muscles so that the absence of the enzyme reduces inflammation. The analysis of macrophage populations indicates that these events depend on the altered polarization of M1 macrophages towards an M2 phenotype. Our results unravel a novel role of ASMase in regulating immune response during muscle regeneration/repair and suggest ASMase as a supplemental therapeutic target in conditions of redundant inflammation that impairs muscle recovery.
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Fujimaki, Shin, Masanao Machida, Tamami Wakabayashi, Makoto Asashima, Tohru Takemasa, and Tomoko Kuwabara. "Functional Overload Enhances Satellite Cell Properties in Skeletal Muscle." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/7619418.
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Skeletal muscle represents a plentiful and accessible source of adult stem cells. Skeletal-muscle-derived stem cells, termed satellite cells, play essential roles in postnatal growth, maintenance, repair, and regeneration of skeletal muscle. Although it is well known that the number of satellite cells increases following physical exercise, functional alterations in satellite cells such as proliferative capacity and differentiation efficiency following exercise and their molecular mechanisms remain unclear. Here, we found that functional overload, which is widely used to model resistance exercise, causes skeletal muscle hypertrophy and converts satellite cells from quiescent state to activated state. Our analysis showed that functional overload induces the expression of MyoD in satellite cells and enhances the proliferative capacity and differentiation potential of these cells. The changes in satellite cell properties coincided with the inactivation of Notch signaling and the activation of Wnt signaling and likely involve modulation by transcription factors of the Sox family. These results indicate the effects of resistance exercise on the regulation of satellite cells and provide insight into the molecular mechanism of satellite cell activation following physical exercise.
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Shen, Linyuan, Tianci Liao, Jingyun Chen, Jianfeng Ma, Jinyong Wang, Lei Chen, Shunhua Zhang, et al. "Genistein Promotes Skeletal Muscle Regeneration by Regulating miR-221/222." International Journal of Molecular Sciences 23, no. 21 (November 3, 2022): 13482. http://dx.doi.org/10.3390/ijms232113482.
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Genistein (GEN), a phytoestrogen, has been reported to regulate skeletal muscle endocrine factor expression and muscle fiber type switching, but its role in skeletal muscle regeneration is poorly understood. As a class of epigenetic regulators widely involved in skeletal muscle development, microRNAs (miRNAs) have the potential to treat skeletal muscle injury. In this study, we identified miR-221 and miR-222 and their target genes MyoG and Tnnc1 as key regulators during skeletal muscle regeneration, and both were regulated by GEN. C2C12 myoblasts and C2C12 myotubes were then used to simulate the proliferation and differentiation of muscle satellite cells during skeletal muscle regeneration. The results showed that GEN could inhibit the proliferation of satellite cells and promote the differentiation of satellite cells by inhibiting the expression of miR-221/222. Subsequent in vitro and in vivo experiments showed that GEN improved skeletal muscle regeneration mainly by promoting satellite cell differentiation in the middle and late stages, by regulating miR-221/222 expression. These results suggest that miR-221/222 and their natural regulator GEN have potential applications in skeletal muscle regeneration.
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Clow, Charlene, and Bernard J. Jasmin. "Brain-derived Neurotrophic Factor Regulates Satellite Cell Differentiation and Skeltal Muscle Regeneration." Molecular Biology of the Cell 21, no. 13 (July 2010): 2182–90. http://dx.doi.org/10.1091/mbc.e10-02-0154.
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In adult skeletal muscle, brain-derived neurotrophic factor (BDNF) is expressed in myogenic progenitors known as satellite cells. To functionally address the role of BDNF in muscle satellite cells and regeneration in vivo, we generated a mouse in which BDNF is specifically depleted from skeletal muscle cells. For comparative purposes, and to determine the specific role of muscle-derived BDNF, we also examined muscles of the complete BDNF−/− mouse. In both models, expression of the satellite cell marker Pax7 was significantly decreased. Furthermore, proliferation and differentiation of primary myoblasts was abnormal, exhibiting delayed induction of several markers of differentiation as well as decreased myotube size. Treatment with exogenous BDNF protein was sufficient to rescue normal gene expression and myotube size. Because satellite cells are responsible for postnatal growth and repair of skeletal muscle, we next examined whether regenerative capacity was compromised. After injury, BDNF-depleted muscle showed delayed expression of several molecular markers of regeneration, as well as delayed appearance of newly regenerated fibers. Recovery of wild-type BDNF levels was sufficient to restore normal regeneration. Together, these findings suggest that BDNF plays an important role in regulating satellite cell function and regeneration in vivo, particularly during early stages.
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Jackson, Janna R., Jyothi Mula, Tyler J. Kirby, Christopher S. Fry, Jonah D. Lee, Margo F. Ubele, Kenneth S. Campbell, John J. McCarthy, Charlotte A. Peterson, and Esther E. Dupont-Versteegden. "Satellite cell depletion does not inhibit adult skeletal muscle regrowth following unloading-induced atrophy." American Journal of Physiology-Cell Physiology 303, no. 8 (October 15, 2012): C854—C861. http://dx.doi.org/10.1152/ajpcell.00207.2012.
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Resident muscle stem cells, known as satellite cells, are thought to be the main mediators of skeletal muscle plasticity. Satellite cells are activated, replicate, and fuse into existing muscle fibers in response to both muscle injury and mechanical load. It is generally well-accepted that satellite cells participate in postnatal growth, hypertrophy, and muscle regeneration following injury; however, their role in muscle regrowth following an atrophic stimulus remains equivocal. The current study employed a genetic mouse model (Pax7-DTA) that allowed for the effective depletion of >90% of satellite cells in adult muscle upon the administration of tamoxifen. Vehicle and tamoxifen-treated young adult female mice were either hindlimb suspended for 14 days to induce muscle atrophy or hindlimb suspended for 14 days followed by 14 days of reloading to allow regrowth, or they remained ambulatory for the duration of the experimental protocol. Additionally, 5-bromo-2′-deoxyuridine (BrdU) was added to the drinking water to track cell proliferation. Soleus muscle atrophy, as measured by whole muscle wet weight, fiber cross-sectional area, and single-fiber width, occurred in response to suspension and did not differ between satellite cell-depleted and control muscles. Furthermore, the depletion of satellite cells did not attenuate muscle mass or force recovery during the 14-day reloading period, suggesting that satellite cells are not required for muscle regrowth. Myonuclear number was not altered during either the suspension or the reloading period in soleus muscle fibers from vehicle-treated or satellite cell-depleted animals. Thus, myonuclear domain size was reduced following suspension due to decreased cytoplasmic volume and was completely restored following reloading, independent of the presence of satellite cells. These results provide convincing evidence that satellite cells are not required for muscle regrowth following atrophy and that, instead, the myonuclear domain size changes as myofibers adapt.
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Bischoff, R. "Interaction between satellite cells and skeletal muscle fibers." Development 109, no. 4 (August 1, 1990): 943–52. http://dx.doi.org/10.1242/dev.109.4.943.
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Single myofibers with attached satellite cells isolated from adult rats were used to study the influence of the mature myofiber on the proliferation of satellite cells. The satellite cells remain quiescent when cultured in serum containing medium but proliferate when exposed to mitogen from an extract of crushed adult muscle. The response of satellite cells to mitogen was measured under three situations with respect to cell contact: (1) in contact with a viable myofiber and its basal lamina, (2) detached from the myofiber by centrifugal force and deposited on the substratum and (3) beneath the basal lamina of a Marcaine killed myofiber. The results show that satellite cells in contact with the plasmalemma of a viable myofiber have reduced mitogenic response. Since inhibiting growth may induce differentiation, I tested whether satellite cells proliferating on the surface of a myofiber would fuse. Although the satellite cell progeny were fusion competent, they did not fuse with the myofiber. To determine whether fusion competence of the myofiber changes with time in culture, embryonic myoblasts were challenged to fuse with myofibers that had been stripped of satellite cells and cultured for several days. The myoblasts fused with pseudopodial sprouts growing from the ends of the myofiber, but did not fuse with the original myofiber surface. These results indicate that contact with the surface of a mature myofiber suppresses proliferation of myogenic cells but the cells do not fuse with the myofiber.
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Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "Molecular Regulation and Rejuvenation of Muscle Stem (Satellite) Cell Aging." Indonesian Biomedical Journal 7, no. 2 (August 1, 2015): 73. http://dx.doi.org/10.18585/inabj.v7i2.73.
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BACKGROUND: Age-related muscle loss leads to lack of muscle strength, resulting in reduced posture and mobility and an increased risk of falls, all of which contribute to a decrease in quality of life. Skeletal muscle regeneration is a complex process, which is not yet completely understood.CONTENT: Skeletal muscle undergoes a progressive age-related loss in mass and function. Preservation of muscle mass depends in part on satellite cells, the resident stem cells of skeletal muscle. Reduced satellite cell function may contribute to the age-associated decrease in muscle mass. Recent studies have delineated that the aging process in organ stem cells is largely caused by age-specific changes in the differentiated niches, and that regenerative outcomes often depend on the age of the niche, rather than on stem cell age. It is likely that epigenetic states will be better define such key satellite cell features as prolonged quiescence and lineage fidelity. It is also likely that DNA and histone modifications will underlie many of the changes in aged satellite cells that account for age-related declines in functionality and rejuvenation through exposure to the systemic environment.SUMMARY: Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Decreased muscle stem cell function in aging has long been shown to depend on altered environmental cues, whereas the contribution of intrinsic mechanisms remained less clear. Signals in the aged niche were shown to cause permanent defects in the ability of satellite cells to return to quiescence, ultimately also impairing the maintenance of self-renewing satellite cells. Therefore, only anti-aging strategies taking both factors, the stem cell niche and the stem cells per se, into consideration may ultimately be successful.KEYWORDS: satellite cell, muscle, aging, niche, regenerations
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Braga, Melissa, Zena Simmons, Keith C. Norris, Monica G. Ferrini, and Jorge N. Artaza. "Vitamin D induces myogenic differentiation in skeletal muscle derived stem cells." Endocrine Connections 6, no. 3 (April 2017): 139–50. http://dx.doi.org/10.1530/ec-17-0008.
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Skeletal muscle wasting is a serious disorder associated with health conditions such as aging, chronic kidney disease and AIDS. Vitamin D is most widely recognized for its regulation of calcium and phosphate homeostasis in relation to bone development and maintenance. Recently, vitamin D supplementation has been shown to improve muscle performance and reduce the risk of falls in vitamin D deficient older adults. However, little is known of the underlying molecular mechanism(s) or the role it plays in myogenic differentiation. We examined the effect of 1,25-D3 on myogenic cell differentiation in skeletal muscle derived stem cells. Primary cultures of skeletal muscle satellite cells were isolated from the tibialis anterior, soleus and gastrocnemius muscles of 8-week-old C57/BL6 male mice and then treated with 1,25-D3. The efficiency of satellite cells isolation determined by PAX7+ cells was 81%, and they expressed VDR. Incubation of satellite cells with 1,25-D3 induces increased expression of: (i) MYOD, (ii) MYOG, (iii) MYC2, (iv) skeletal muscle fast troponin I and T, (v) MYH1, (vi) IGF1 and 2, (vii) FGF1 and 2, (viii) BMP4, (ix) MMP9 and (x) FST. It also promotes myotube formation and decreases the expression of MSTN. In conclusion, 1,25-D3 promoted a robust myogenic effect on satellite cells responsible for the regeneration of muscle after injury or muscle waste. This study provides a mechanistic justification for vitamin D supplementation in conditions characterized by loss of muscle mass and also in vitamin D deficient older adults with reduced muscle mass and strength, and increased risk of falls.
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Mesires, N. T., and M. E. Doumit. "Satellite cell proliferation and differentiation during postnatal growth of porcine skeletal muscle." American Journal of Physiology-Cell Physiology 282, no. 4 (April 1, 2002): C899—C906. http://dx.doi.org/10.1152/ajpcell.00341.2001.
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Age-related changes in satellite cell proliferation and differentiation during rapid growth of porcine skeletal muscle were examined. Satellite cells were isolated from hindlimb muscles of pigs at 1, 7, 14, and 21 wk of age (4 animals/age group). Satellite cells were separated from cellular debris by using Percoll gradient centrifugation and were adsorbed to glass coverslips for fluorescent immunostaining. Positive staining for neural cell adhesion molecule (NCAM) distinguished satellite cells from nonmyogenic cells. The proportion of NCAM-positive cells (satellite cells) in isolates decreased from 1 to 7 wk of age. Greater than 77% of NCAM-positive cells were proliferating cell nuclear antigen positive at all ages studied. Myogenin-positive satellite cells decreased from 30% at 1 wk to 14% at 7 wk of age and remained at constant levels thereafter. These data indicate that a high percentage of satellite cells remain proliferative during rapid postnatal muscle growth. The reduced proportion of myogenin-positive cells during growth may reflect a decrease in the proportion of differentiating satellite cells or accelerated incorporation of myogenin-positive cells into myofibers.
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Li, Yi-Ping. "TNF-α is a mitogen in skeletal muscle." American Journal of Physiology-Cell Physiology 285, no. 2 (August 2003): C370—C376. http://dx.doi.org/10.1152/ajpcell.00453.2002.
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Emerging evidence suggests that tumor necrosis factor (TNF)-α plays a role in muscle repair. To determine whether TNF-α modulates satellite cell proliferation, the current study evaluated TNF-α effects on DNA synthesis in primary myoblasts and on satellite cell activation in adult mouse muscle. Exposure to recombinant TNF-α increased total DNA content in rat primary myoblasts dose-dependently over a 24-h period and increased the number of primary myoblasts incorporating 5-bromo-2′-deoxyuridine (BrdU) during a 30-min pulse labeling. Systemic injection of TNF-α stimulated BrdU incorporation by satellite cells in muscles of adult mice, whereas no BrdU was incorporated by satellite cells in control mice. TNF-α stimulated serum response factor (SRF) binding to the serum response element (SRE) present in the c- fos gene promoter and stimulated reporter gene expression controlled by the same element. Our data suggest that TNF-α activates satellite cells to enter the cell cycle and accelerates G1-to-S phase transition, and these actions may involve activation of early response genes via SRF.
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Zhao, Jing, Xiaoxu Shen, Xinao Cao, Haorong He, Shunshun Han, Yuqi Chen, Can Cui, et al. "HDAC4 Regulates the Proliferation, Differentiation and Apoptosis of Chicken Skeletal Muscle Satellite Cells." Animals 10, no. 1 (January 4, 2020): 84. http://dx.doi.org/10.3390/ani10010084.
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The development of skeletal muscle satellite cells (SMSCs) is a complex process that could be regulated by many genes. Previous studies have shown that Histone Deacetylase 4 (HDAC4) plays a critical role in cell proliferation, differentiation, and apoptosis in mouse. However, the function of HDAC4 in chicken muscle development is still unknown. Given that chicken is a very important meat-producing animal that is also an ideal model to study skeletal muscle development, we explored the functions of HDAC4 in chicken SMSCs after the interference of HDAC4. The results showed that HDAC4 was enriched in embryonic skeletal muscle, and it was highly expressed in embryonic muscle than in postnatal muscles. Meanwhile, knockdown of HDAC4 could significantly inhibit the proliferation and differentiation of chicken SMSCs but had no effect on the apoptosis of SMSCs as observed in a series of experiment conducted in vitro. These results indicated that HDAC4 might play a positive role in chicken skeletal muscle growth and development.
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Manole, Emilia, Gisela Gaina, Laura Cristina Ceafalan, and Mihail Eugen Hinescu. "Skeletal Muscle Stem Cells in Aging: Asymmetric/Symmetric Division Switching." Symmetry 14, no. 12 (December 17, 2022): 2676. http://dx.doi.org/10.3390/sym14122676.
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In aged muscle, satellite cells’ symmetric and asymmetric divisions are impaired, and intrinsic and extrinsic complex mechanisms govern these processes. This review presents many updated aspects regarding muscle stem cells’ fate in normal and aging conditions. The balance between self-renewal and commitment divisions contributes to muscle regeneration, muscle homeostasis, aging, and disease. Stimulating muscle regeneration in aging could be a therapeutic target, but there is still a need to understand the many mechanisms that influence each other in satellite cells and their niche. We highlight here the general outlines regarding satellite cell divisions, the primary markers present in muscle stem cells, the aging aspects concerning signaling pathways involved in symmetric/asymmetric divisions, the regenerative capacity of satellite cells and their niche alteration in senescent muscle, genetics and epigenetics mechanisms implied in satellite cells aging and exercise effect on muscle regeneration in the elderly.
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Chen, William, David Datzkiw, and Michael A. Rudnicki. "Satellite cells in ageing: use it or lose it." Open Biology 10, no. 5 (May 2020): 200048. http://dx.doi.org/10.1098/rsob.200048.
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Individuals that maintain healthy skeletal tissue tend to live healthier, happier lives as proper muscle function enables maintenance of independence and actuation of autonomy. The onset of skeletal muscle decline begins around the age of 30, and muscle atrophy is associated with a number of serious morbidities and mortalities. Satellite cells are responsible for regeneration of skeletal muscle and enter a reversible non-dividing state of quiescence under homeostatic conditions. In response to injury, satellite cells are able to activate and re-enter the cell cycle, creating new cells to repair and create nascent muscle fibres while preserving a small population that can return to quiescence for future regenerative demands. However, in aged muscle, satellite cells that experience prolonged quiescence will undergo programmed cellular senescence, an irreversible non-dividing state that handicaps the regenerative capabilities of muscle. This review examines how periodic activation and cycling of satellite cells through exercise can mitigate senescence acquisition and myogenic decline.
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Malatesta, Manuela, Federica Perdoni, Sylviane Muller, Carlo Pellicciari, and Carlo Zancanaro. "Pre-mRNA Processing Is Partially Impaired in Satellite Cell Nuclei from Aged Muscles." Journal of Biomedicine and Biotechnology 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/410405.
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Satellite cells are responsible for the capacity of mature mammalian skeletal muscles to repair and maintain mass. During aging, skeletal muscle mass as well as the muscle strength and endurance progressively decrease, leading to a condition termed sarcopenia. The causes of sarcopenia are manifold and remain to be completely elucidated. One of them could be the remarkable decline in the efficiency of muscle regeneration; this has been associated with decreasing amounts of satellite cells, but also to alterations in their activation, proliferation, and/or differentiation. In this study, we investigated the satellite cell nuclei of biceps and quadriceps muscles from adult and old rats; morphometry and immunocytochemistry at light and electron microscopy have been combined to assess the organization of the nuclear RNP structural constituents involved in different steps of mRNA formation. We demonstrated that in satellite cells the RNA pathways undergo alterations during aging, possibly hampering their responsiveness to muscle damage.
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Doyle, Michelle J., Sheng Zhou, Kathleen Kelly Tanaka, Addolorata Pisconti, Nicholas H. Farina, Brian P. Sorrentino, and Bradley B. Olwin. "Abcg2 labels multiple cell types in skeletal muscle and participates in muscle regeneration." Journal of Cell Biology 195, no. 1 (September 26, 2011): 147–63. http://dx.doi.org/10.1083/jcb.201103159.
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Skeletal muscle contains progenitor cells (satellite cells) that maintain and repair muscle. It also contains muscle side population (SP) cells, which express Abcg2 and may participate in muscle regeneration or may represent a source of satellite cell replenishment. In Abcg2-null mice, the SP fraction is lost in skeletal muscle, although the significance of this loss was previously unknown. We show that cells expressing Abcg2 increased upon injury and that muscle regeneration was impaired in Abcg2-null mice, resulting in fewer centrally nucleated myofibers, reduced myofiber size, and fewer satellite cells. Additionally, using genetic lineage tracing, we demonstrate that the progeny of Abcg2-expressing cells contributed to multiple cell types within the muscle interstitium, primarily endothelial cells. After injury, Abcg2 progeny made a minor contribution to regenerated myofibers. Furthermore, Abcg2-labeled cells increased significantly upon injury and appeared to traffic to muscle from peripheral blood. Together, these data suggest an important role for Abcg2 in positively regulating skeletal muscle regeneration.
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Bohnert, Kathryn L., Mary K. Hastings, David R. Sinacore, Jeffrey E. Johnson, Sandra E. Klein, Jeremy J. McCormick, Paul Gontarz, and Gretchen A. Meyer. "Skeletal Muscle Regeneration in Advanced Diabetic Peripheral Neuropathy." Foot & Ankle International 41, no. 5 (February 14, 2020): 536–48. http://dx.doi.org/10.1177/1071100720907035.
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Background: Decreased lean muscle mass in the lower extremity in diabetic peripheral neuropathy (DPN) is thought to contribute to altered joint loading, immobility, and disability. However, the mechanism behind this loss is unknown and could derive from a reduction in size of myofibers (atrophy), destruction of myofibers (degeneration), or both. Degenerative changes require participation of muscle stem (satellite) cells to regenerate lost myofibers and restore lean mass. Determining the degenerative state and residual regenerative capacity of DPN muscle will inform the utility of regeneration-targeted therapeutic strategies. Methods: Biopsies were acquired from 2 muscles in 12 individuals with and without diabetic neuropathy undergoing below-knee amputation surgery. Biopsies were subdivided for histological analysis, transcriptional profiling, and satellite cell isolation and culture. Results: Histological analysis revealed evidence of ongoing degeneration and regeneration in DPN muscles. Transcriptional profiling supports these findings, indicating significant upregulation of regeneration-related pathways. However, regeneration appeared to be limited in samples exhibiting the most severe structural pathology as only extremely small, immature regenerated myofibers were found. Immunostaining for satellite cells revealed a significant decrease in their relative frequency only in the subset with severe pathology. Similarly, a reduction in fusion in cultured satellite cells in this group suggests impairment in regenerative capacity in severe DPN pathology. Conclusion: DPN muscle exhibited features of degeneration with attempted regeneration. In the most severely pathological muscle samples, regeneration appeared to be stymied and our data suggest that this may be partly due to intrinsic dysfunction of the satellite cell pool in addition to extrinsic structural pathology (eg, nerve damage). Clinical Relevance: Restoration of DPN muscle function for improved mobility and physical activity is a goal of surgical and rehabilitation clinicians. Identifying myofiber degeneration and compromised regeneration as contributors to dysfunction suggests that adjuvant cell-based therapies may improve clinical outcomes.
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Guadagnin, Eleonora, Davi Mázala, and Yi-Wen Chen. "STAT3 in Skeletal Muscle Function and Disorders." International Journal of Molecular Sciences 19, no. 8 (August 2, 2018): 2265. http://dx.doi.org/10.3390/ijms19082265.
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Signal transducer and activator of transcription 3 (STAT3) signaling plays critical roles in regulating skeletal muscle mass, repair, and diseases. In this review, we discuss the upstream activators of STAT3 in skeletal muscles, with a focus on interleukin 6 (IL6) and transforming growth factor beta 1 (TGF-β1). We will also discuss the double-edged effect of STAT3 activation in the muscles, including the role of STAT3 signaling in muscle hypertrophy induced by exercise training or muscle wasting in cachectic diseases and muscular dystrophies. STAT3 is a critical regulator of satellite cell self-renewal after muscle injury. STAT3 knock out affects satellite cell myogenic progression by impairing proliferation and inducing premature differentiation. Recent studies in STAT3 signaling demonstrated its direct role in controlling myogenic capacity of myoblasts and satellite cells, as well as the potential benefit in using STAT3 inhibitors to treat muscle diseases. However, prolonged STAT3 activation in muscles has been shown to be responsible for muscle wasting by activating protein degradation pathways. It is important to balance the extent of STAT3 activation and the duration and location (cell types) of the STAT3 signaling when developing therapeutic interventions. STAT3 signaling in other tissues and organs that can directly or indirectly affects skeletal muscle health are also discussed.
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Chakravarthy, Manu V., Bradley S. Davis, and Frank W. Booth. "IGF-I restores satellite cell proliferative potential in immobilized old skeletal muscle." Journal of Applied Physiology 89, no. 4 (October 1, 2000): 1365–79. http://dx.doi.org/10.1152/jappl.2000.89.4.1365.
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One of the key factors responsible for the age-associated reduction in muscle mass may be that satellite cell proliferation potential (number of doublings contained within each cell) could become rate limiting to old muscle regrowth. No studies have tested whether repeated cycles of atrophy-regrowth in aged animals deplete the remaining capacity of satellite cells to replicate or what measures can be taken to prevent this from happening. We hypothesized that there would be a pronounced loss of satellite cell proliferative potential in gastrocnemius muscles of aged rats (25- to 30-mo-old FBN rats) subjected to three cycles of atrophy by hindlimb immobilization (plaster casts) with intervening recovery periods. Our results indicated that there was a significant loss in gastrocnemius muscle mass and in the proliferative potential of the resident satellite cells after just one bout of immobilization. Neither the muscle mass nor the satellite cell proliferation potential recovered from their atrophied values after either the first 3-wk or later 9-wk recovery period. Remarkably, application of insulin-like growth factor I onto the atrophied gastrocnemius muscle for an additional 2 wk after this 9-wk recovery period rescued ∼46% of the lost muscle mass and dramatically increased proliferation potential of the satellite cells from this muscle.
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Scaramozza, Annarita, Valeria Marchese, Valentina Papa, Roberta Salaroli, Gianni Sorarù, Corrado Angelini, and Giovanna Cenacchi. "Skeletal Muscle Satellite Cells in Amyotrophic Lateral Sclerosis." Ultrastructural Pathology 38, no. 5 (July 31, 2014): 295–302. http://dx.doi.org/10.3109/01913123.2014.937842.
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Bischoff, R. "Interaction between Satellite Cells and Skeletal Muscle Fibers." Development 110, no. 3 (November 1, 1990): 653—s—653. http://dx.doi.org/10.1242/dev.110.3.653-s.
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SOETA, Chie, Keitaro YAMANOUCHI, Telhisa HASEGAWA, Nobushige ISHIDA, Harutaka MUKOYAMA, Hideaki TOJO, and Chikashi TACHI. "Isolation of Satellite Cells from Equine Skeletal Muscle." Journal of Equine Science 9, no. 3 (1998): 97–100. http://dx.doi.org/10.1294/jes.9.97.
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Morgan, J. E. "D.I.4 Satellite cells and skeletal muscle regeneration." Neuromuscular Disorders 21, no. 9-10 (October 2011): 640. http://dx.doi.org/10.1016/j.nmd.2011.06.756.
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Molnar, Greg, Nancy A. Schroedl, Steve R. Gonda, and Charles R. Hartzell. "Skeletal muscle satellite cells cultured in simulated microgravity." In Vitro Cellular & Developmental Biology - Animal 33, no. 5 (May 1997): 386–91. http://dx.doi.org/10.1007/s11626-997-0010-9.
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He, Haorong, Huadong Yin, Xueke Yu, Yao Zhang, Menggen Ma, Diyan Li, and Qing Zhu. "PDLIM5 Affects Chicken Skeletal Muscle Satellite Cell Proliferation and Differentiation via the p38-MAPK Pathway." Animals 11, no. 4 (April 4, 2021): 1016. http://dx.doi.org/10.3390/ani11041016.
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Skeletal muscle satellite cell growth and development is a complicated process driven by multiple genes. The PDZ and LIM domain 5 (PDLIM5) gene has been proven to function in C2C12 myoblast differentiation and is involved in the regulation of skeletal muscle development. The role of PDLIM5 in chicken skeletal muscle satellite cells, however, is unclear. In this study, in order to determine whether the PDLIM5 gene has a function in chicken skeletal muscle satellite cells, we examined the changes in proliferation and differentiation of chicken skeletal muscle satellite cells (SMSCs) after interfering and overexpressing PDLIM5 in cells. In addition, the molecular pathways of the PDLIM5 gene regulating SMSC proliferation and differentiation were analyzed by transcriptome sequencing. Our results show that PDLIM5 can promote the proliferation and differentiation of SMSCs; furthermore, through transcriptome sequencing, it can be found that the differential genes are enriched in the MAPK signaling pathway after knocking down PDLIM5. Finally, it was verified that PDLIM5 played an active role in the proliferation and differentiation of chicken SMSCs by activating the p38-MAPK signaling pathway. These results indicate that PDLIM5 may be involved in the growth and development of chicken skeletal muscle.
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Schultz, E., K. C. Darr, and A. Macius. "Acute effects of hindlimb unweighting on satellite cells of growing skeletal muscle." Journal of Applied Physiology 76, no. 1 (January 1, 1994): 266–70. http://dx.doi.org/10.1152/jappl.1994.76.1.266.
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The proliferative behavior of satellite cells in growing rat soleus and extensor digitorum longus muscles was examined at short periods after initiation of hindlimb unweighting. Mitotic activity of satellite cells in both muscles decreased below weight-bearing control levels within 24 h of initiation of hindlimb unweighting. This satellite cell response was > or = 48 h before any atrophic morphological changes that take place in the muscles. Suppression of mitotic activity was most severe in the soleus muscle where continuous infusion of label demonstrated that virtually all mitotic activity was abolished between 3 and 5 days. The results of this study suggest that satellite cell mitotic activity is a sensitive indicator of primary atrophic changes occurring in growing myofibers and may be a predictor of future morphological changes.
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Tatsumi, Ryuichi, Xiaosong Liu, Antonio Pulido, Mark Morales, Tomowa Sakata, Sharon Dial, Akihito Hattori, Yoshihide Ikeuchi, and Ronald E. Allen. "Satellite cell activation in stretched skeletal muscle and the role of nitric oxide and hepatocyte growth factor." American Journal of Physiology-Cell Physiology 290, no. 6 (June 2006): C1487—C1494. http://dx.doi.org/10.1152/ajpcell.00513.2005.
Full textAbstract:
In the present study, we examined the roles of hepatocyte growth factor (HGF) and nitric oxide (NO) in the activation of satellite cells in passively stretched rat skeletal muscle. A hindlimb suspension model was developed in which the vastus, adductor, and gracilis muscles were subjected to stretch for 1 h. Satellite cells were activated by stretch determined on the basis of 5-bromo-2′-deoxyuridine (BrdU) incorporation in vivo. Extracts from stretched muscles stimulated BrdU incorporation in freshly isolated control rat satellite cells in a concentration-dependent manner. Extracts from stretched muscles contained the active form of HGF, and the satellite cell-activating activity could be neutralized by incubation with anti-HGF antibody. The involvement of NO was investigated by administering nitro-l-arginine methyl ester (l-NAME) or the inactive enantiomer NG-nitro-d-arginine methyl ester HCl (d-NAME) before stretch treatment. In vivo activation of satellite cells in stretched muscle was not inhibited by d-NAME but was inhibited by l-NAME. The activity of stretched muscle extract was abolished by l-NAME treatment but could be restored by the addition of HGF, indicating that the extract was not inhibitory. Finally, NO synthase activity in stretched and unstretched muscles was assayed in muscle extracts immediately after 2-h stretch treatment and was found to be elevated in stretched muscle but not in stretched muscle from l-NAME-treated rats. The results of these experiments demonstrate that stretching muscle liberates HGF in a NO-dependent manner, which can activate satellite cells.