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Статті в журналах з теми "Muscle cells"

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Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 10 березня 2023

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1

Griffin, D. M., H. M. Hudson, A. Belhaj-Saïf, B. J. McKiernan, and P. D. Cheney. "Do Corticomotoneuronal Cells Predict Target Muscle EMG Activity?" Journal of Neurophysiology 99, no. 3 (March 2008): 1169–986. http://dx.doi.org/10.1152/jn.00906.2007.

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Data from two rhesus macaques were used to investigate the pattern of cortical cell activation during reach-to-grasp movements in relation to the corresponding activation pattern of the cell's facilitated target muscles. The presence of postspike facilitation (PSpF) in spike-triggered averages (SpTAs) of electromyographic (EMG) activity was used to identify cortical neurons with excitatory synaptic linkages with motoneurons. EMG activity from 22 to 24 muscles of the forelimb was recorded together with the activity of M1 cortical neurons. The extent of covariation was characterized by 1) identifying the task segment containing the cell and target muscle activity peaks, 2) quantifying the timing and overlap between corticomotoneuronal (CM) cell and EMG peaks, and 3) applying Pearson correlation analysis to plots of CM cell firing rate versus EMG activity of the cell's facilitated muscles. At least one firing rate peak, for nearly all (95%) CM cells tested, matched a corresponding peak in the EMG activity of the cell's target muscles. Although some individual CM cells had very strong correlations with target muscles, overall, substantial disparities were common. We also investigated correlations for ensembles of CM cells sharing the same target muscle. The ensemble population activity of even a small number of CM cells influencing the same target muscle produced a relatively good match ( r ≥ 0.8) to target muscle EMG activity. Our results provide evidence in support of the notion that corticomotoneuronal output from primary motor cortex encodes movement in a framework of muscle-based parameters, specifically muscle-activation patterns as reflected in EMG activity.

2

Reyes, Morayma, and Jeffrey S. Chamberlain. "Perivascular CD45−:Sca-1+:CD34− Cells Are Derived from Bone Marrow Cells and Participate in Dystrophic Skeletal Muscle Regeneration." Blood 106, no. 11 (November 16, 2005): 394. http://dx.doi.org/10.1182/blood.v106.11.394.394.

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Abstract Multiple mechanisms may account for bone marrow (BM) cell incorporation into myofibers following muscle damage. Here, we demonstrated that CD45−:Sca-1+:CD34− cells may play a role in the regeneration of mdx4cv skeletal muscles, an animal model for Duchenne muscular dystrophy. To understand the origin of CD45−:Sca-1+:CD34− cells in skeletal muscle, we reconstituted lethally irradiated wild type (wt) or mdx4cv mice with unfractionated BM cells from transgenic mice ubiquitously expressing green fluorescence protein (GFP). 1, 2, and 6 months post-transplantation, we analyzed the skeletal muscle mononuclear cells from the recipients by flow cytometry for GFP, CD45-PerCP, Sca-1-PE, and CD34-APC. To our surprise, we found a small percentage of BM-derived (GFP+) CD45−:Sca-1+:CD34− cells in the skeletal muscles of these GFP+ BM transplant recipients. These BM-derived cells are localized in the perivascular tissue by immunostaining and their frequency increases with time. We were interested in the potential of these cells for clinical application for muscle diseases. Thus, we FACS-sorted CD45−:Sca-1+:CD34− cells from GFP transgenic mouse skeletal muscles and transplanted them in the tibialis anterior (TA) muscle of mdx4cv mice. In ten days we found significant muscle engraftment. In addition, we studied the response of this population upon acute muscle injury. For this, we injected cardiotoxin in the right TA muscle of mdx4cv and wt mice, followed by BrdU administration in drinking water for three days. After 3.5 days, mice were sacrificed and the right and left (control) TA muscles were harvested and muscle CD45−:Sca-1+:CD34− cells were FACS-sorted, fixed and stained for BrdU and Myf-5. In the injured muscle (right TA), more than 70% of these cells were BrdU+ and more than 50% were Myf-5+, compared to baseline levels (close to zero) in the left TA. This indicates that this population can undergo proliferation and myogenic commitment upon muscle injury. To understand how these BM cells migrate to the muscle and once in the muscle how they mobilize, we investigated the in vitro chemotatic response of GFP+ (BM derived) CD45−:Sca-1+ cells isolated from muscles of GFP+ BM transplant recipients. We found that these cells were highly chemoattrated to stroma derived factor, SDF-1, a chemo-attractant for cells expressing CXCR4. We also observed higher frequency of BM-derived CD45−:Sca-1+:CD34− cells in dystrophic muscle than wt muscle, which may be explained by higher expression levels of SDF-1 in dystrophic muscles. In an effort to determine the identity of these cells when ex vivo cultured, we cultured them in several stem cell media, including a low-serum medium containing specific cytokines for the isolation and expansion of multipotent adult progenitor cells (MAPCs). MAPCs can be isolated from skeletal muscle and BM and can differentiate into multiple tissue cells. Strikingly, we found that MAPCs were enriched up to 40 folds by sorting this population from skeletal muscle. The frequency of BM-derived muscle MAPCs also increases with time post-transplantation in dystrophic muscles. These BM-derived muscle MAPCs displayed the typical MAPC immunophenotypes, displayed a normal diploid karyotype and were capable to differentiate into endothelial cells, hepatocytes and neurons. Taken together, our results suggest that dystrophic muscles recruit BM cells that localize in perivascular tissues and can be defined as CD45-:Sca-1+:CD34-. This population when cultured enriches for MAPCs and can participate in muscle regeneration in dystrophic muscles.

3

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.

4

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.

5

Balch, Ying. "Subculture human skeletal muscle cells to produce the cells with different Culture medium compositions." Clinical Research and Clinical Trials 3, no. 4 (April 30, 2021): 01–03. http://dx.doi.org/10.31579/2693-4779/036.

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This study aimed to subculture human skeletal muscle cells (HSkMC) using a culture medium with different compositions to determine the most efficient medium for the growth of the human skeletal muscle cells. The culture media was divided into three groups: Group1. An HSkMC growth medium. Group 2. An HSkMC growth medium + with 10% high glucose (GH). Group 3. An HSkMC growth medium + 10% fetal bovine serum (FBS). HSkMC from groups 1 to 3 gradually became round in shape and gathered in clusters. These changes differed between the groups. In group 3, the HSkMC clusters were more in numbers and gathered as significantly more prominent than in the other groups under the EVOS-Microscope shown. We concluded that by manipulating the composition of the culture medium, it is possible to induce HSkMC to promote the best growth.

6

Mitchell, Patrick O., and Grace K. Pavlath. "Skeletal muscle atrophy leads to loss and dysfunction of muscle precursor cells." American Journal of Physiology-Cell Physiology 287, no. 6 (December 2004): C1753—C1762. http://dx.doi.org/10.1152/ajpcell.00292.2004.

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Atrophy of skeletal muscle leads to decreases in myofiber size and nuclear number; however, the effects of atrophic conditions on muscle precursor cells (MPC) are largely unknown. MPC lie outside myofibers and represent the main source of additional myonuclei necessary for muscle growth and repair. In the present study, we examined the properties of MPC after hindlimb suspension (HS)-induced atrophy and subsequent recovery of the mouse hindlimb muscles. We demonstrated that the number of MPC in atrophied muscles was decreased. RT-PCR analysis of cells isolated from atrophied muscles indicated that several mRNA characteristic of the myogenic program in MPC were absent. Cells isolated from atrophied muscles failed to properly proliferate and undergo differentiation into multinucleated myotubes. Thus atrophy led to a decrease in MPC and caused dysfunction in those MPC that remained. Upon regrowth of the atrophied muscles, these deleterious effects were reversed. Our data suggest that preventing loss or dysfunction of MPC may be a new pharmacological target during muscle atrophy.

7

Becker, S., G. Pasca, D. Strumpf, L. Min, and T. Volk. "Reciprocal signaling between Drosophila epidermal muscle attachment cells and their corresponding muscles." Development 124, no. 13 (July 1, 1997): 2615–22. http://dx.doi.org/10.1242/dev.124.13.2615.

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Directed intercellular interactions between distinct cell types underlie the basis for organogenesis during embryonic development. This paper focuses on the establishment of the final somatic muscle pattern in Drosophila, and on the possible cross-talk between the myotubes and the epidermal muscle attachment cells, occurring while both cell types undergo distinct developmental programs. Our findings suggest that the stripe gene is necessary and sufficient to initiate the developmental program of epidermal muscle attachment cells. In stripe mutant embryos, these cells do not differentiate correctly. Ectopic expression of Stripe in various epidermal cells transforms these cells into muscle-attachment cells expressing an array of epidermal muscle attachment cell-specific markers. Moreover, these ectopic epidermal muscle attachment cells are capable of attracting somatic myotubes from a limited distance, providing that the myotube has not yet been attached to or been influenced by a closer wild-type attachment cell. Analysis of the relationships between muscle binding and differentiation of the epidermal muscle attachment cell was performed in mutant embryos in which loss of muscles, or ectopic muscles were induced. This analysis indicated that, although the initial expression of epidermal muscle-attachment cell-specific genes including stripe and groovin is muscle independent, their continuous expression is maintained only in epidermal muscle attachment cells that are connected to muscles. These results suggest that the binding of a somatic muscle to an epidermal muscle attachment cell triggers a signal affecting gene expression in the attachment cell. Taken together, our results suggest the presence of a reciprocal signaling mechanism between the approaching muscles and the epidermal muscle attachment cells. First the epidermal muscle attachment cells signal the myotubes and induce myotube attraction and adhesion to their target cells. Following this binding, the muscle cells send a reciprocal signal to the epidermal muscle attachment cells inducing their terminal differentiation into tendon-like cells.

8

Challa, Stalin Reddy, and Swathi Goli. "Differentiation of Human Embryonic Stem Cells into Engrafting Myogenic Precursor Cells." Stem cell Research and Therapeutics International 1, no. 1 (April 16, 2019): 01–05. http://dx.doi.org/10.31579/2643-1912/002.

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Degenerative muscle diseases affect muscle tissue integrity and function. Human embryonic stem cells (hESC) are an attractive source of cells to use in regenerative therapies due to their unlimited capacity to divide and ability to specialize into a wide variety of cell types. A practical way to derive therapeutic myogenic stem cells from hESC is lacking. In this study, we demonstrate the development of two serum-free conditions to direct the differentiation of hESC towards a myogenic precursor state. Using TGFß and PI3Kinase inhibitors in combination with bFGF we showed that one week of differentiation is sufficient for hESC to specialize into PAX3+/PAX7+ myogenic precursor cells. These cells also possess the capacity to further differentiate in vitro into more specialized myogenic cells that express MYOD, Myogenin, Desmin and MYHC, and showed engraftment in vivo upon transplantation in immunodeficient mice. Ex vivo myomechanical studies of dystrophic mouse hindlimb muscle showed functional improvement one month post-transplantation. In summary, this study describes a promising system to derive engrafting muscle precursor cells solely using chemical substances in serum-free conditions and without genetic manipulation.

9

Morgan, Jennifer E., and Terence A. Partridge. "Muscle satellite cells." International Journal of Biochemistry & Cell Biology 35, no. 8 (August 2003): 1151–56. http://dx.doi.org/10.1016/s1357-2725(03)00042-6.

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10

Visan, Ioana. "Muscle Treg cells." Nature Immunology 15, no. 2 (January 21, 2014): 142. http://dx.doi.org/10.1038/ni.2818.

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11

Tedgui, Alain, and Ziad Mallat. "Smooth Muscle Cells." Circulation Research 87, no. 2 (July 21, 2000): 81–82. http://dx.doi.org/10.1161/01.res.87.2.81.

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12

Feige, Peter, and Michael A. Rudnicki. "Muscle stem cells." Current Biology 28, no. 10 (May 2018): R589—R590. http://dx.doi.org/10.1016/j.cub.2018.02.064.

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13

Relaix, Frédéric, and Christophe Marcelle. "Muscle stem cells." Current Opinion in Cell Biology 21, no. 6 (December 2009): 748–53. http://dx.doi.org/10.1016/j.ceb.2009.10.002.

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14

Goldring, Kirstin, Terence Partridge, and Diana Watt. "Muscle stem cells." Journal of Pathology 197, no. 4 (2002): 457–67. http://dx.doi.org/10.1002/path.1157.

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15

Heslop, L., J. E. Morgan, and T. A. Partridge. "Evidence for a myogenic stem cell that is exhausted in dystrophic muscle." Journal of Cell Science 113, no. 12 (June 15, 2000): 2299–308. http://dx.doi.org/10.1242/jcs.113.12.2299.

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Injection of the myotoxin notexin, was found to induce regeneration in muscles that had been subjected to 18 Gy of radiation. This finding was unexpected as irradiation doses of this magnitude are known to block regeneration in dystrophic (mdx) mouse muscle. To investigate this phenomenon further we subjected mdx and normal (C57Bl/10) muscle to irradiation and notexin treatment and analysed them in two ways. First by counting the number of newly regenerated myofibres expressing developmental myosin in cryosections of damaged muscles. Second, by isolating single myofibres from treated muscles and counting the number of muscle precursor cells issuing from these over 2 day and 5 day periods. After irradiation neither normal nor dystrophic muscles regenerate to any significant extent. Moreover, single myofibres cultured from such muscles produce very few muscle precursor cells and these undergo little or no proliferation. However, when irradiated normal and mdx muscles were subsequently treated with notexin, regeneration was observed. In addition, some of the single myofibres produced rapidly proliferative muscle precursor cells when cultured. This occurred more frequently, and the myogenic cells proliferated more extensively, with fibres cultured from normal compared with dystrophic muscles. Even after 25 Gy, notexin induced some regeneration but no proliferative myogenic cells remained associated with the muscle fibres. Thus, skeletal muscles contain a number of functionally distinct populations of myogenic cells. Most are radiation sensitive. However, some survive 18 Gy as proliferative myogenic cells that can be evoked by extreme conditions of muscle damage; this population is markedly diminished in muscles of the mdx mouse. A small third population survives 25 Gy and forms muscle but not proliferative myogenic cells.

16

Sanders, Kenton M., Sean M. Ward, and Sang Don Koh. "Interstitial Cells: Regulators of Smooth Muscle Function." Physiological Reviews 94, no. 3 (July 2014): 859–907. http://dx.doi.org/10.1152/physrev.00037.2013.

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Smooth muscles are complex tissues containing a variety of cells in addition to muscle cells. Interstitial cells of mesenchymal origin interact with and form electrical connectivity with smooth muscle cells in many organs, and these cells provide important regulatory functions. For example, in the gastrointestinal tract, interstitial cells of Cajal (ICC) and PDGFRα+cells have been described, in detail, and represent distinct classes of cells with unique ultrastructure, molecular phenotypes, and functions. Smooth muscle cells are electrically coupled to ICC and PDGFRα+cells, forming an integrated unit called the SIP syncytium. SIP cells express a variety of receptors and ion channels, and conductance changes in any type of SIP cell affect the excitability and responses of the syncytium. SIP cells are known to provide pacemaker activity, propagation pathways for slow waves, transduction of inputs from motor neurons, and mechanosensitivity. Loss of interstitial cells has been associated with motor disorders of the gut. Interstitial cells are also found in a variety of other smooth muscles; however, in most cases, the physiological and pathophysiological roles for these cells have not been clearly defined. This review describes structural, functional, and molecular features of interstitial cells and discusses their contributions in determining the behaviors of smooth muscle tissues.

17

Zikic, Dragan, Slobodan Stojanovic, Mirjana Djukic-Stojcic, Zdenko Kanacki, Verica Milosevic, and Gordana Uscebrka. "Morphological characteristics of breast and thigh muscles of slow- and medium growing strains of chickens." Biotehnologija u stocarstvu 32, no. 1 (2016): 27–35. http://dx.doi.org/10.2298/bah1601027z.

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Morphological characteristics of skeletal muscles of slow- and medium-growing strains of chickens are very important for meat quality and comparison with fast-growing strains. The aim of this paper was to evaluate morphological parameters of breast and thigh muscles of slow- and mediumgrowing strains in a free-range system. The slow-growing strains used in the experiment were autochthonous breeds Sombor crested and Banat naked neck, and the medium-growing strain was Red-bro. The tissue samples were taken from the thigh muscle and muscles of the breast of 10 chickens of each breed. Samples were stained with hematoxylin - eosin and enzyme succinate - dehydrogenase (SDH). The following morphological parameters were observed: diameter of muscle cells, nucleo-cytoplasmic ratio of muscle cells, volume density of connective tissue within the muscle and the presence of red, white and intermediate muscle cell types. Between strains, the type of muscle or genotype didn?t have significant effects on diameters of muscle cells and nucleo-cytoplasmic ratio in the muscle cells. Results indicated that genotype had significant effect on volume density of the connective tissue in breast muscles. Red muscle cells were, in all strains, significantly more represented in m. biceps femoris than m. pectoralis superficialis. Genotype had significant effect on ratio between connective tissue and muscle cells and no significant effects on other morphological parameters.

18

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.

19

Fukuda, K., Y. Tanigawa, G. Fujii, S. Yasugi, and S. Hirohashi. "cFKBP/SMAP; a novel molecule involved in the regulation of smooth muscle differentiation." Development 125, no. 18 (September 15, 1998): 3535–42. http://dx.doi.org/10.1242/dev.125.18.3535.

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During embryogenesis, smooth muscle cells of the gut differentiate from mesenchymal cells derived from splanchnic mesoderm. We have isolated a gene involved in the differentiation of smooth muscle cells in the gut using differential display between the chicken proventriculus in which the smooth muscle layer develops poorly and the gizzard in which smooth muscles develop abundantly. The protein encoded by this gene showed highest similarity to mouse FK506 binding protein, FKBP65, and from the function of this protein it was designated chicken FKBP/smooth muscle activating protein (cFKBP/SMAP). cFKBP/SMAP was first expressed in smooth muscle precursor cells of the gut and, after smooth muscles differentiate, expression was restricted to smooth muscle cells. In organ culture of the gizzard, the differentiation of smooth muscle cells was inhibited by the addition of FK506, the inhibitor of FKBPs. Moreover, overexpression of cFKBP/SMAP in lung and gizzard mesenchymal cells induced smooth muscle differentiation. In addition, cFKBP/SMAP-induced smooth muscle differentiation was inhibited by FK506. We postulate therefore that cFKBP/SMAP plays a crucial role in smooth muscle differentiation in the gut and provides a powerful tool to study smooth muscle differentiation mechanisms, which have been poorly analyzed so far.

20

Szewczyk, N. J., J. J. Hartman, S. J. Barmada, and L. A. Jacobson. "Genetic defects in acetylcholine signalling promote protein degradation in muscle cells of Caenorhabditis elegans." Journal of Cell Science 113, no. 11 (June 1, 2000): 2003–10. http://dx.doi.org/10.1242/jcs.113.11.2003.

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A myosin-lacZ fusion, expressed in 103 muscle cells of Caenorhabditis elegans, reports on how proteolysis in muscle is controlled by neural and intramuscular signals. Upon acute starvation, the fusion protein is degraded in the posterior 63 cells of the body-wall muscle, but remains stable in 32 anterior body-wall muscles and 8 vulval muscle cells. This distinction correlates with differences in the innervation of these cells. Reporter protein in the head and vulval muscles becomes labile upon genetic ‘denervation’ in mutants that have blocks in pre-synaptic synthesis or release of acetylcholine (ACh) or post-synaptic reception at nicotinic ACh receptors (nAChR), whereas protein in all 103 muscles is stabilized by the nicotinic agonist levamisole in the absence of ACh production. Levamisole does not stabilize muscle protein in nAChR mutants that are behaviorally resistant to levamisole. Neural inputs thus exert negative control over the proteolytic process in muscle by stimulating muscle nicotinic ACh receptors.

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Carvajal Monroy, P. L., S. Grefte, A. M. Kuijpers-Jagtman, J. W. Von den Hoff, and F. A. D. T. G. Wagener. "Neonatal Satellite Cells Form Small Myotubes In Vitro." Journal of Dental Research 96, no. 3 (November 19, 2016): 331–38. http://dx.doi.org/10.1177/0022034516679136.

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Although palatal muscle reconstruction in patients with cleft palate takes place during early childhood, normal speech development is often not achieved. We hypothesized that the intrinsic properties of head satellite cells (SCs) and the young age of these patients contribute to the poor muscle regeneration after surgery. First, we studied the fiber type distribution and the expression of SC markers in ex vivo muscle tissue from head (branchiomeric) and limb (somite-derived) muscles from neonatal (2-wk-old) and young (9-wk-old) rats. Next, we cultured SCs isolated from these muscles for 5, 7, and 9 d, and investigated the in vitro expression of SC markers, as well as changes in proliferation, early differentiation, and fusion index (myotube formation) in these cells. In our ex vivo samples, we found that virtually all myofibers in both the masseter (Mass) and the levator veli palatini (LVP) muscles contained fast myosin heavy chain (MyHC), and a small percentage of digastric (Dig) and extensor digitorum longus myofibers also contained slow MyHC. This was independent of age. More SCs were found in muscles from neonatal rats as compared with young rats [17.6 (3.8%) v. 2.3 (1.6%); P < 0.0001]. In vitro, young branchiomeric head muscle (BrHM) SCs proliferated longer and differentiated later than limb muscle SCs. No differences were found between SC cultures from the different BrHMs. SC cultures from neonatal muscles showed a much higher proliferation index than those from young animals at 5 d (0.8 v. 0.2; P < 0.001). In contrast, the fusion index in neonate SCs was about twice as low as that in SCs from young muscles at 9 d [27.6 (1.4) v. 62.8 (10.2), P < 0.0001]. In conclusion, SCs from BrHM differ from limb muscles especially in their delayed differentiation. SCs from neonatal muscles form myotubes less efficiently than those from young muscles. These age-dependent differences in stem cell properties urge careful consideration for future clinical applications in patients with cleft palate.

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Ardizzi, J. P., and H. F. Epstein. "Immunochemical localization of myosin heavy chain isoforms and paramyosin in developmentally and structurally diverse muscle cell types of the nematode Caenorhabditis elegans." Journal of Cell Biology 105, no. 6 (December 1, 1987): 2763–70. http://dx.doi.org/10.1083/jcb.105.6.2763.

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The nematode Caenorhabditis elegans contains two major groups of muscle cells that exhibit organized sarcomeres: the body wall and pharyngeal muscles. Several additional groups of muscle cells of more limited mass and spatial distribution include the vulval muscles of hermaphrodites, the male sex muscles, the anal-intestinal muscles, and the gonadal sheath of the hermaphrodite. These muscle groups do not exhibit sarcomeres and therefore may be considered smooth. Each muscle cell has been shown to have a specific origin in embryonic cell lineages and differentiation, either embryonically or postembryonically (Sulston, J. E., and H. R. Horvitz. 1977. Dev. Biol. 56:110-156; Sulston, J. E., E. Schierenberg, J. White, and J. N. Thomson. 1983. Dev. Biol. 100:64-119). Each muscle type exhibits a unique combination of lineage and onset of differentiation at the cellular level. Biochemically characterized monoclonal antibodies to myosin heavy chains A, B, C, and D and to paramyosin have been used in immunochemical localization experiments. Paramyosin is detected by immunofluorescence in all muscle cells. Myosin heavy chains C and D are limited to the pharyngeal muscle cells, whereas myosin heavy chains A and B are localized not only within the sarcomeres of body wall muscle cells, as reported previously, but to the smooth muscle cells of the minor groups as well. Myosin heavy chains A and B and paramyosin proteins appear to be compatible with functionally and structurally distinct muscle cell types that arise by multiple developmental pathways.

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Motohashi, Norio, Matthew S. Alexander, and Louis M. Kunkel. "Skeletal muscle regeneration and muscle progenitor cells." Journal of Physical Fitness and Sports Medicine 1, no. 1 (2012): 151–54. http://dx.doi.org/10.7600/jpfsm.1.151.

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24

Dezawa, M. "Bone Marrow Stromal Cells Generate Muscle Cells and Repair Muscle Degeneration." Science 309, no. 5732 (July 8, 2005): 314–17. http://dx.doi.org/10.1126/science.1110364.

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25

Mañas-García, Laura, Maria Guitart, Xavier Duran, and Esther Barreiro. "Satellite Cells and Markers of Muscle Regeneration during Unloading and Reloading: Effects of Treatment with Resveratrol and Curcumin." Nutrients 12, no. 6 (June 23, 2020): 1870. http://dx.doi.org/10.3390/nu12061870.

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We hypothesized that treatment with pharmacological agents known to increase sirtuin-1 activity (resveratrol and curcumin) may enhance muscle regeneration. In limb muscles of mice (C57BL/6J, 10 weeks) exposed to reloading for seven days following a seven-day period of hindlimb immobilization with/without curcumin or resveratrol treatment, progenitor muscle cell numbers (FACS), satellite cell subtypes (histology), early and late muscle regeneration markers, phenotype and morphometry, sirtuin-1 activity and content, and muscle function were assessed. Treatment with either resveratrol or curcumin in immobilized muscles elicited a significant improvement in numbers of progenitor, activated, quiescent, and total counts of muscle satellite cells, compared to non-treated animals. Treatment with either resveratrol or curcumin in reloaded muscles compared to non-treated mice induced a significant improvement in the CSA of both hybrid (curcumin) and fast-twitch fibers (resveratrol), sirtuin-1 activity (curcumin), sirtuin-1 content (resveratrol), and counts of progenitor muscle cells (resveratrol). Treatment with the pharmacological agents resveratrol and curcumin enhanced the numbers of satellite cells (muscle progenitor, quiescent, activated, and total satellite cells) in the unloaded limb muscles but not in the reloaded muscles. These findings have potential clinical implications as treatment with these phenolic compounds would predominantly be indicated during disuse muscle atrophy to enhance the muscle regeneration process.

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Torrente, Yuan, Jacques-P. Tremblay, Federica Pisati, Marzia Belicchi, Barbara Rossi, Manuela Sironi, Franco Fortunato, et al. "Intraarterial Injection of Muscle-Derived Cd34+Sca-1+ Stem Cells Restores Dystrophin in mdx Mice." Journal of Cell Biology 152, no. 2 (January 22, 2001): 335–48. http://dx.doi.org/10.1083/jcb.152.2.335.

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Duchenne muscular dystrophy is a lethal recessive disease characterized by widespread muscle damage throughout the body. This increases the difficulty of cell or gene therapy based on direct injections into muscles. One way to circumvent this obstacle would be to use circulating cells capable of homing to the sites of lesions. Here, we showed that stem cell antigen 1 (Sca-1), CD34 double-positive cells purified from the muscle tissues of newborn mice are multipotent in vitro and can undergo both myogenic and multimyeloid differentiation. These muscle-derived stem cells were isolated from newborn mice expressing the LacZ gene under the control of the muscle-specific desmin or troponin I promoter and injected into arterial circulation of the hindlimb of mdx mice. The ability of these cells to interact and firmly adhere to endothelium in mdx muscles microcirculation was demonstrated by intravital microscopy after an intraarterial injection. Donor Sca-1, CD34 muscle-derived stem cells were able to migrate from the circulation into host muscle tissues. Histochemical analysis showed colocalization of LacZ and dystrophin expression in all muscles of the injected hindlimb in all of five out of five 8-wk-old treated mdx mice. Their participation in the formation of muscle fibers was significantly increased by muscle damage done 48 h after their intraarterial injection, as indicated by the presence of 12% β-galactosidase–positive fibers in muscle cross sections. Normal dystrophin transcripts detected enzymes in the muscles of the hind limb injected intraarterially by the mdx reverse transcription polymerase chain reaction method, which differentiates between normal and mdx message. Our results showed that the muscle-derived stem cells first attach to the capillaries of the muscles and then participate in regeneration after muscle damage.

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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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Watanabe, T., H. Hosoya, and S. Yonemura. "1P205 Live imaging of Non-muscle myosin II in epithelial cells." Seibutsu Butsuri 45, supplement (2005): S83. http://dx.doi.org/10.2142/biophys.45.s83_1.

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29

Connor, E. A., and U. J. McMahan. "Cell accumulation in the junctional region of denervated muscle." Journal of Cell Biology 104, no. 1 (January 1, 1987): 109–20. http://dx.doi.org/10.1083/jcb.104.1.109.

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If skeletal muscles are denervated, the number of mononucleated cells in the connective tissue between muscle fibers increases. Since interstitial cells might remodel extracellular matrix, and since extracellular matrix in nerve and muscle plays a direct role in reinnervation of the sites of the original neuromuscular junctions, we sought to determine whether interstitial cell accumulation differs between junctional and extrajunctional regions of denervated muscle. We found in muscles from frog and rat that the increase in interstitial cell number was severalfold (14-fold for frog, sevenfold for rat) greater in the vicinity of junctional sites than in extrajunctional regions. Characteristics of the response at the junctional sites of frog muscles are as follows. During chronic denervation, the accumulation of interstitial cells begins within 1 wk and it is maximal by 3 wk. Reinnervation 1-2 wk after nerve damage prevents the maximal accumulation. Processes of the cells form a multilayered veil around muscle fibers but make little, if any, contact with the muscle cell or its basal lamina sheath. The results of additional experiments indicate that the accumulated cells do not originate from terminal Schwann cells or from muscle satellite cells. Most likely the cells are derived from fibroblasts that normally occupy the space between muscle fibers and are known to make and degrade extracellular matrix components.

30

Torrente, Y., M. Belicchi, C. Marchesi, G. D'antona, F. Cogiamanian, F. Pisati, M. Gavina, et al. "Autologous Transplantation of Muscle-Derived CD133+ Stem Cells in Duchenne Muscle Patients." Cell Transplantation 16, no. 6 (July 2007): 563–77. http://dx.doi.org/10.3727/000000007783465064.

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Duchenne muscular dystrophy (DMD) is a lethal X-linked recessive muscle disease due to defect on the gene encoding dystrophin. The lack of a functional dystrophin in muscles results in the fragility of the muscle fiber membrane with progressive muscle weakness and premature death. There is no cure for DMD and current treatment options focus primarily on respiratory assistance, comfort care, and delaying the loss of ambulation. Recent works support the idea that stem cells can contribute to muscle repair as well as to replenishment of the satellite cell pool. Here we tested the safety of autologous transplantation of muscle-derived CD133+ cells in eight boys with Duchenne muscular dystrophy in a 7-month, double-blind phase I clinical trial. Stem cell safety was tested by measuring muscle strength and evaluating muscle structures with MRI and histological analysis. Timed cardiac and pulmonary function tests were secondary outcome measures. No local or systemic side effects were observed in all treated DMD patients. Treated patients had an increased ratio of capillary per muscle fibers with a switch from slow to fast myosin-positive myofibers.

31

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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Brohmann, H., K. Jagla, and C. Birchmeier. "The role of Lbx1 in migration of muscle precursor cells." Development 127, no. 2 (January 15, 2000): 437–45. http://dx.doi.org/10.1242/dev.127.2.437.

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The homeobox gene Lbx1 is expressed in migrating hypaxial muscle precursor cells during development. These precursors delaminate from the lateral edge of the dermomyotome and form distinct streams that migrate over large distances, using characteristic paths. The targets of migration are limbs, septum transversum and the floor of the first branchial arch where the cells form skeletal muscle of limbs and shoulders, diaphragm and hypoglossal cord, respectively. We used gene targeting to analyse the function of Lbx1 in the mouse. Myogenic precursor cells delaminate from the dermomyotome in Lbx1 mutants, but migrate in an aberrant manner. Most critically affected are migrating cells that move to the limbs. Precursor cells that reach the dorsal limb field are absent. In the ventral limb, precursors are present but distributed in an abnormal manner. As a consequence, at birth some muscles in the forelimbs are completely lacking (extensor muscles) or reduced in size (flexor muscles). Hindlimb muscles are affected strongly, and distal limb muscles are more affected than proximal ones. Other migrating precursor cells heading towards the floor of the first branchial arch move along the appropriate path in Lbx1 mutants. However, these cells migrate less efficiently and reduced numbers of precursors reach their distal target. At birth, the internal lingual muscle is therefore reduced in size. We suggest that Lbx1 controls the expression of genes that are essential for the recognition or interpretation of cues that guide migrating muscle precursors and maintain their migratory potential.

33

Morawin, Barbara, and Agnieszka Zembroń-Łacny. "Role of endocrine factors and stem cells in skeletal muscle regeneration." Postępy Higieny i Medycyny Doświadczalnej 75 (June 2, 2021): 371–84. http://dx.doi.org/10.5604/01.3001.0014.9125.

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The process of reconstructing damaged skeletal muscles involves degeneration, inflammatory and immune responses, regeneration and reorganization, which are regulated by a number of immune-endocrine factors affecting muscle cells and satellite cells (SCs). One of these molecules is testosterone (T), which binds to the androgen receptor (AR) to initiate the expression of the muscle isoform of insulin-like growth factor 1 (IGF-1Ec). The interaction between T and IGF-1Ec stimulates the growth and regeneration of skeletal muscles by inhibiting apoptosis, enhancement of SCs proliferation and myoblasts differentiation. As a result of sarcopenia, muscle dystrophy or wasting diseases, the SCs population is significantly reduced. Regular physical exercise attenuates a decrease in SCs count, and thus elevates the regenerative potential of muscles in both young and elderly people. One of the challenges of modern medicine is the application of SCs and extracellular matrix scaffolds in regenerative and molecular medicine, especially in the treatment of degenerative diseases and post-traumatic muscle reconstruction. The aim of the study is to present current information on the molecular and cellular mechanisms of skeletal muscle regenera,tion, the role of testosterone and growth factors in the activation of SCs and the possibility of their therapeutic use in stimulating the reconstruction of damaged muscle fibers.

34

Sanders, Kenton M., Yoshihiko Kito, Sung Jin Hwang, and Sean M. Ward. "Regulation of Gastrointestinal Smooth Muscle Function by Interstitial Cells." Physiology 31, no. 5 (September 2016): 316–26. http://dx.doi.org/10.1152/physiol.00006.2016.

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Interstitial cells of mesenchymal origin form gap junctions with smooth muscle cells in visceral smooth muscles and provide important regulatory functions. In gastrointestinal (GI) muscles, there are two distinct classes of interstitial cells, c-Kit+interstitial cells of Cajal and PDGFRα+cells, that regulate motility patterns. Loss of these cells may contribute to symptoms in GI motility disorders.

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Cevik, Hilal, Isabelle Gangadin, Justin G. Boyer, Douglas Millay, and Stephen N. Waggoner. "Key contribution of NK cells to inflammation after muscle injury." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 165.14. http://dx.doi.org/10.4049/jimmunol.208.supp.165.14.

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Abstract Immune activation after tissue injury is required for removal of dead cells and debris to permit subsequent regenerative healing. Natural killer (NK) cells are innate lymphocytes that are essential for immune defense and for regulation of inflammation. NK cells limit fibrosis after cardiac muscle damage, yet the role of these cells during skeletal muscle inflammation is less clear. We hypothesize that NK cells promote acute inflammation after muscle damage but that NK cell responses must be resolved to permit regenerative healing. Following bilateral injection of cardiotoxin into tibialis anterior and gastrocnemius muscles of C57BL/6 mice, NK cell accumulation in injured muscle was detectable within 18 hours and peaked four days post-injury. Selective depletion of NK cells using a titrated dose of anti-NK1.1 antibody prior to cardiotoxin injection resulted in a substantial reduction in the overall infiltration of numerous immune cell types, including T and B cells, into the injured muscle. Thus, NK cells are an important mediator of cellular inflammation following muscle damage. Future studies will determine the mechanism by which NK cells contribute to this inflammatory response and how ablation of NK-cell mediated inflammation impacts healing of damaged muscles. Supported by National Institute of Heath (NIH) (R01-AI148080)

36

Basson, Michael. "Immune cells muscle up." Nature Medicine 19, no. 5 (May 2013): 547. http://dx.doi.org/10.1038/nm.3209.

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37

Cao, Baohong, and Johnny Huard. "Muscle-Derived Stem Cells." Cell Cycle 3, no. 2 (February 2004): 101–4. http://dx.doi.org/10.4161/cc.3.2.644.

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38

LeBrasseur, Nicole. "Muscle cells take heart." Journal of Cell Biology 169, no. 1 (April 4, 2005): 16. http://dx.doi.org/10.1083/jcb1691rr1.

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39

Jankowski, R. J., B. M. Deasy, and J. Huard. "Muscle-derived stem cells." Gene Therapy 9, no. 10 (May 2002): 642–47. http://dx.doi.org/10.1038/sj.gt.3301719.

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40

Van Epps, Heather L. "Muscle cells under attack." Journal of Experimental Medicine 201, no. 4 (February 21, 2005): 487. http://dx.doi.org/10.1084/jem2014iti3.

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41

Watt, D. J., J. Karasinski, J. Moss, and M. A. England. "Migration of muscle cells." Nature 368, no. 6470 (March 1994): 406–7. http://dx.doi.org/10.1038/368406a0.

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42

Fukuda, Daiju, and Masanori Aikawa. "Intimal Smooth Muscle Cells." Circulation 122, no. 20 (November 16, 2010): 2005–8. http://dx.doi.org/10.1161/circulationaha.110.986968.

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Littlewood, Trevor D., and Martin R. Bennett. "Foxing Smooth Muscle Cells." Circulation Research 100, no. 3 (February 16, 2007): 302–4. http://dx.doi.org/10.1161/01.res.0000259101.39931.d3.

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44

Buckingham, Margaret, and Didier Montarras. "Skeletal muscle stem cells." Current Opinion in Genetics & Development 18, no. 4 (August 2008): 330–36. http://dx.doi.org/10.1016/j.gde.2008.06.005.

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45

COOPER, R., G. BUTLERBROWNE, and V. MOULY. "Human muscle stem cells." Current Opinion in Pharmacology 6, no. 3 (June 2006): 295–300. http://dx.doi.org/10.1016/j.coph.2006.01.007.

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46

Hirschi, Karen K., and Mark W. Majesky. "Smooth muscle stem cells." Anatomical Record 276A, no. 1 (2003): 22–33. http://dx.doi.org/10.1002/ar.a.10128.

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47

Hampton, Tracy. "Creating Cardiac Muscle Cells." JAMA 307, no. 5 (February 1, 2012): 446. http://dx.doi.org/10.1001/jama.2012.70.

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48

Harfe, B. D., C. S. Branda, M. Krause, M. J. Stern, and A. Fire. "MyoD and the specification of muscle and non-muscle fates during postembryonic development of the C. elegans mesoderm." Development 125, no. 13 (July 1, 1998): 2479–88. http://dx.doi.org/10.1242/dev.125.13.2479.

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Basic-helix-loop helix factors of the myoD/myf5/ myogenin/MRF4 family have been implicated in acquisition and elaboration of muscle cell fates. Here we describe both myogenic and non-myogenic roles for the Caenorhabditis elegans member of this family (CeMyoD) in postembryonic mesodermal patterning. The postembryonic mesodermal lineage in C. elegans provides a paradigm for many of the issues in mesodermal fate specification: a single mesoblast ('M') divides to generate 14 striated muscles, 16 non-striated muscles, and two non-muscle cells. To study CeMyoD function in the M lineage, we needed to circumvent an embryonic requirement for the protein. Two approaches were used: (1) isolation of mutants that decrease CeMyoD levels while retaining viability, and (2) analysis of genetic mosaics that had lost CeMyoD in the M lineage. With either manipulation, we observed a series of cell-fate transformations affecting a subset of both striated muscles and non-muscle cells. In place of these normal fates, the affected lineages produced a number of myoblast-like cells that initially failed to differentiate, instead swelling to acquire a resemblance to sex myoblasts (M-lineage-derived precursors to non-striated uterine and vulval muscles). Like normal sex myoblasts, the ectopic myoblast-like cells were capable of migration and proliferation followed by differentiation of progeny cells into vulval and uterine muscle. Our results demonstrate a cell-intrinsic contribution of CeMyoD to specification of both non-muscle and muscle fates.

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Boscolo Sesillo, Francesca, Michelle Wong, Amy Cortez, and Marianna Alperin. "Isolation of muscle stem cells from rat skeletal muscles." Stem Cell Research 43 (March 2020): 101684. http://dx.doi.org/10.1016/j.scr.2019.101684.

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50

Morgan, J. E., G. R. Coulton, and T. A. Partridge. "Muscle precursor cells invade and repopulate freeze-killed muscles." Journal of Muscle Research and Cell Motility 8, no. 5 (October 1987): 386–96. http://dx.doi.org/10.1007/bf01578428.

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