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Skeletal Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The increase in fiber size is called hypertrophy. Muscle disuse and loss of innervation, as in paralysis, causes a severe loss of muscle tissue, referred to as muscle atrophy. The increase in the number of muscle fibers is hyperplasia. This has been demonstrated in laboratory animals, such as birds, rats, and cats, as a result of some form of exercise or prolonged electrical stimulation. There are claims that hyperplasia also occurs in humans through two possible mechanisms: (i) splitting of large fibers into two or more smaller fibers, and (ii) fusion of myoblasts to form a new fiber. The myoblasts arise through cell division of satellite cells that are involved in the repair of muscle tissue, as mentioned earlier.
Tissue Engineering and Cell Therapies for Neurogenic Bladder Augmentation and Urinary Continence Restoration
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Other groups investigated the impact of the cell preparation process on myoblast survival.18,20–24 The few animal studies comparing injections of myoblasts with or without prior culturing consistently showed deleterious effects of culture conditions. Enzymatic disaggregation of muscle biopsies was a major cause of MPC death following implantation.20 MPC exposure to culture conditions may also contribute to loss of myogenic potential.23 Montarras et al. found that culturing prior to transplantation markedly reduced the regenerative efficiency of MPCs, so that culture expansion seemed to constitute an “empty” process yielding the same amount of muscle as the number of cells from which the culture was initiated.18 Thus, there is evidence that the myogenic potential of injected MPCs can be impaired by the cell preparation process, most notably the enzyme digestion step, and by cell culture conditions. It remained to be determined whether injecting small numbers of cells without previous cultivation is more effective than injecting large numbers of MPCs previously expanded in vitro.
Metabolic Therapies for Muscle Injury
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Ana V. Cintrón, Kenneth Cintron
Research has been focused on muscle satellite cells (SC) and their role in muscle repair and regeneration. They are skeletal muscle mononuclear stem cells, which remain in a quiescent state until activation occurs in response to different physiological and pathological stimuli, including exercise, stretching, electrical stimulation and injury such as post-training micro-injuries [77]. Activation results in the formation of precursor myogenic cells known as myoblasts, which are responsible for muscle fiber hypertrophy through the addition of nuclei to existing myofibers [18]. They also have an important implication in cell therapy due to their self-renewal as well as their capability to differentiate into myofibers, processes which depend on a number of factors, including the microenvironment and the presence of myogenic regulatory factors.
Muscle regeneration after high-dose radiation exposure: therapeutic potential of Hedgehog pathway modulation?
Published in International Journal of Radiation Biology, 2022
E. Rota Graziosi, S. François, J. Pateux, M. Gauthier, X. Butigieg, M. Oger, M. Drouet, D. Riccobono, N. Jullien
Muscle repair is a complex process that involves the regeneration of damaged fibers by new ones formed from particular stem cells identified in 1961 by Mauro and known as satellite cells (SC) (Mauro 1961; Zammit et al. 2006). These progenitors, interspersed between the plasma membrane and the basal layer of fibers, can be activated from their quiescent state following a traumatic event to proliferate and differentiate into mature myoblasts, which fuze to reconstitute myotubes. These newly-formed structures merge into myofibers and regenerate a functional muscle. The different stages of differentiation, fusion and maturation are orchestrated by a cascade of myogenic regulatory factors (MRF). SC markers Pax3 and Pax7 disappear after the early stages of activation. Then, in the intermediate stages, Myf5 and MyoD are necessary for myoblast commitment toward muscle cell differentiation. Myogenin (MyoG gene) plays a role in the late phases of fusion and in the synthesis of Myosin, essential for muscle functionality (Hawke and Garry 2001). Other mature proteins are also synthesized at the end of the process, such as beta-enolase (ENO3 gene) which is involved especially in the storage of glycogen.
Proteomic profiling of carbonic anhydrase CA3 in skeletal muscle
Published in Expert Review of Proteomics, 2021
Paul Dowling, Stephen Gargan, Margit Zweyer, Hemmen Sabir, Dieter Swandulla, Kay Ohlendieck
Isoform CA3 can be considered a mesodermal marker of development [77]. The diversification of contractile fibers during development and tissue plasticity are cellular hallmarks of the skeletal musculature. The process of myogenesis is initially characterized by the cellular commitment to the highly specialized skeletal muscle lineage, which is then followed by myogenic differentiation, myoblast fusion, and myotube formation to establish multi-nucleated contractile fibers and the development of mature motor units [78]. The complex specification steps of muscle development require the partially overlapping activity of myogenic transcription factors in combination with neuronal stimulation patterns to produce physiologically functional nerve–muscle interactions and fiber type distribution within individual skeletal muscles [79]. During early myogenesis, expression of CA3 occurs at the level of the notochord and the somites and then increases in all maturing skeletal muscles [80].
Synergistic effect of glucocorticoids and IGF-1 on myogenic differentiation through the Akt/GSK-3β pathway in C2C12 myoblasts
Published in International Journal of Neuroscience, 2020
Xiao-Bo Fang, Zu-Biao Song, Meng-Shu Xie, Yan-Mei Liu, Wei-Xi Zhang
Quiescent satellite cells are muscle precursors located between the skeletal muscle sarcolemma and basement membrane that proliferate in response to muscle injury or exercise, resulting in muscle recovery and more satellite cells [10]. Myogenesis is a highly coordinated developmental process in which satellite cells first commit to the myogenic lineage and to proliferation. Then, myoblasts withdraw from the cell cycle, differentiate to express muscle-specific genes and, finally, fuse to multinucleated myotubes [11]. This process, also referred to as myogenic differentiation, is regulated by the transcription factor MyoD as well as by other myogenic regulatory factors (MRFs), including myogenin, MRF4 and Myf5 [11,12]. MyoD and Myf5 are expressed at the initiation of myogenic specification, while myogenin and MRF4 are related to the terminal process of differentiation and myotube formation [7,9]. Previous studies have revealed that insulin growth factor-1 (IGF-1) is critical for normal muscle growth and development in vivo [13,14]. However, IGF-1 levels in both circulating and muscle cells often decrease in response to glucocorticoids [15]. Moreover, IGF-1 is known to prevent glucocorticoid-induced muscle atrophy in myotubes, but the effects of glucocorticoids combined with IGF-1 on myogenesis have rarely been reported. Therefore, we hypothesized that glucocorticoids together with IGF-1 can enhance myogenic differentiation.