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Collection and Expansion of Stem Cells
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Normal repair and regeneration of skeletal muscle fibers occurs following injury from muscle satellite cell activation, proliferation and migration to the site of injury.164 Satellite cells are a unique population of usually quiescent cells located outside of the myofiber, between the sarcolemma and the covering basement membrane, and account for approximately 5% of the nuclei present in muscle fibers. When activated, satellite cells have the capacity to divide extensively in order to produce sufficient myoblasts to replace damaged muscle fiber. Recovery of satellite cells via standard tissue dissociation techniques, fail to extract more that 99% of the known myogenic population of mature muscle,165 bringing into question the number of cell types that contribute to muscle development in vivo. Satellite cells attached to muscle fibers are capable of rapid proliferation and myogenesis in tissue culture,165 but when transplanted in vivo into recipient murine muscle, the majority of cultured cells undergo rapid necrotic cell death.166 Only a few cells survive to give rise to regenerated myofibers and satellite cells. More stringent techniques for identifying myogenic precursors within muscle and tracing their fate are required to determine the spectrum of cell types responsible for skeletal muscle regeneration in vivo.
Molecular Mechanisms of Training Effects
Published in Atko Viru, Adaptation in Sports Training, 2017
Specialized cells must contain an array of positive and negative regulators that modify the actions of transcriptional activators.120 Recently, the family of myogenic factors (myogenesis-controlling genes) was discovered. This family includes myoD, myogens, MRF-1, and Myf-5, which are expressed in skeletal muscle cells. They activate the myogenic program in fibroblasts. All these proteins activate their own transcription in transfected cells. They influence also the transcription of other proteins. The muscle-specific enhancer regions contain binding-sites for regulatory proteins as well as MyoD.121
Tissue engineering and cell therapies for neurogenic bladder augmentation and urinary continence restoration
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
The cells involved in regenerating adult skeletal muscle are believed to closely resemble the cells involved in myogenesis. During embryogenesis, the somites give rise to successive waves of myoblasts, which colonize the limbs within the first 18 days after conception. These myoblasts fuse into primary myotubes, which eventually mature into myofibers. A subset of myoblasts sequestered in a quiescent state between the basal lamina and the sarcolemma, known as satellite cells, ensures muscle repair in adulthood. Satellite cells constitute the main population of MPCs. In the event of muscle injury, the satellite cells proliferate and differentiate into secondary myoblasts, which fuse into new myotubes or repair the parental myofibers (Figure 52.4).
History of Drosophila neurogenetic research in South Korea
Published in Journal of Neurogenetics, 2023
Greg S. B. Suh, Kweon Yu, Young-Joon Kim, Yangkyun Oh, Joong-Jean Park
As the primary interest of the field transitioned from early embryogenesis to tissue and organ development and pattern formation, South Korea witnessed the emergence of highly talented scientists who made critical contributions to the field. For example, Jaeseob Kim discovered that vestigial gene is required for wing development and, intriguingly, is sufficient to induce the development of wing tissues in any organ, such as eyes or legs, when it is expressed ectopically in these organs (Kim et al., 1996). Such a breakthrough led to further development of the concept of a ‘master regulator’ for organ development. Just as wing development was found to be governed by vestigial gene, Walter Gehring’s laboratory discovered that the development of eye is governed by eyeless gene (Halder, Callaerts, & Gehring, 1995). Just a half decade earlier, investigators had observed a simpler master regulator that was able to induce the development of a specific cell type. Myogenesis, for instance, was found to be induced by the expression of a single gene MyoD (Tapscott et al., 1988). It was not yet conceivable, however, that an entire organ consisting of different cell types could be induced and reconstituted through the ectopic expression of a single gene. This novel concept of the master regulator has influenced enormously – in the fields of mammalian development, stem cell, and organ regeneration years to come.
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].
Role of acute exacerbations in skeletal muscle impairment in COPD
Published in Expert Review of Respiratory Medicine, 2021
Harry R. Gosker, Ramon C. Langen, Sami O. Simons
The actions of pro-inflammatory cytokines like TNFα, IL-1β and IFNγ on skeletal muscle have been well-documented in a variety of experimental settings. Raising circulatory levels of TNFα artificially using transgenic mice, or by implantation of TNFα- or IFNγ-secreting tumors, results in skeletal muscle dysfunction and atrophy of both limb and respiratory muscles [84–88]. Cell studies using cultured myotubes (in vitro myofiber surrogates) have demonstrated that inflammatory cytokines directly impact on skeletal muscle. Administration of combinations of TNFα, IL-1, and IFNγ, or TNFα alone to myotube cultures is sufficient to induce atrophy [89,90]. Cytokine-driven muscle dysfunction involves increased proteolysis mediated by E3 Ub-ligases including MuRF1 and Atrogin-1 [91,92]. In addition, inflammatory cytokines impair satellite (i.e. muscle progenitor) cell-dependent myogenesis by affecting essential regulatory molecules like MyoD [89,93]. NF-κB activation has been shown as a required step in inflammation-induced muscle atrophy, both in vitro and in vivo, and muscle-specific activation of NF-κB using genetic modification is sufficient to induce a strong muscle wasting phenotype [89,94,95]. Pro-inflammatory cytokines also cause a reduction in muscle OXPHEN, which primarily appears to rely on reduced mitochondrial biogenesis [96,97]. Moreover, TNFα or IL-1-elicited loss of OXPHEN requires NF-κB activation, implicating this intracellular inflammatory signaling pathway as a central mediator of inflammation-induced muscle dysfunction [98].