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Seminars in Cell & Developmental Biology Jul 2023Mitochondria play a major role in apoptotic signaling. In addition to its role in eliminating dysfunctional cells, mitochondrial apoptotic signaling is implicated as a... (Review)
Review
Mitochondria play a major role in apoptotic signaling. In addition to its role in eliminating dysfunctional cells, mitochondrial apoptotic signaling is implicated as a key component of myogenic differentiation and skeletal muscle atrophy. For example, the activation of cysteine-aspartic proteases (caspases; CASP's) can aid in the initial remodeling stages of myogenic differentiation by cleaving protein kinases, transcription factors, and cytoskeletal proteins. Precise regulation of these signals is needed to prevent excessive cell disassemble and subsequent cell death. During skeletal muscle atrophy, the activation of CASP's and mitochondrial derived nucleases participate in myonuclear fragmentation, a potential loss of myonuclei, and cleavage of contractile structures within skeletal muscle. The B cell leukemia/lymphoma 2 (BCL2) family of proteins play a significant role in regulating myogenesis and skeletal muscle atrophy by governing the initiating steps of mitochondrial apoptotic signaling. This review discusses the role of mitochondrial apoptotic signaling in skeletal muscle remodeling during myogenic differentiation and skeletal muscle pathological states, including aging, disuse, and muscular dystrophy.
Topics: Humans; Apoptosis; Caspases; Muscle Development; Muscle, Skeletal; Muscular Atrophy; Mitochondria, Muscle
PubMed: 35241367
DOI: 10.1016/j.semcdb.2022.01.011 -
TheScientificWorldJournal 2013Recent studies have shown that mitochondria play a role in the regulation of myogenesis. Indeed, the abundance, morphology, and functional properties of mitochondria... (Review)
Review
Recent studies have shown that mitochondria play a role in the regulation of myogenesis. Indeed, the abundance, morphology, and functional properties of mitochondria become altered when the myoblasts differentiate into myotubes. For example, mitochondrial mass/volume, mtDNA copy number, and mitochondrial respiration are markedly increased after the onset of myogenic differentiation. Besides, mitochondrial enzyme activity is also increased, suggesting that the metabolic shift from glycolysis to oxidative phosphorylation as the major energy source occurs during myogenic differentiation. Several lines of evidence suggest that impairment of mitochondrial function and activity blocks myogenic differentiation. However, yet little is known about the molecular mechanisms underlying the regulation of myogenesis by mitochondria. Understanding how mitochondria are involved in myogenesis will provide a valuable insight into the underlying mechanisms that regulate the maintenance of cellular homeostasis. Here, we will summarize the current knowledge regarding the role of mitochondria as a potential regulator of myogenesis.
Topics: Animals; Cell Differentiation; DNA, Mitochondrial; Gene Expression Regulation; Genome, Mitochondrial; Glycolysis; Humans; Mitochondria; Muscle Development; Oxidative Phosphorylation; Regeneration; Transcription, Genetic
PubMed: 23431256
DOI: 10.1155/2013/593267 -
Experimental Cell Research Mar 2023
Topics: Muscle Development; Muscle, Skeletal; Cell Differentiation
PubMed: 36608838
DOI: 10.1016/j.yexcr.2023.113457 -
Biomedicine & Pharmacotherapy =... Sep 2023Cordycepin (with a molecular formula of CHNO), a natural adenosine isolated from Cordyceps militaris, has an important regulatory effect on skeletal muscle remodelling...
Cordycepin (with a molecular formula of CHNO), a natural adenosine isolated from Cordyceps militaris, has an important regulatory effect on skeletal muscle remodelling and quality maintenance. The aim of this study was to investigate the effect of cordycepin on myoblast differentiation and explore the underlying molecular mechanisms of this effect. Our results showed that cordycepin inhibited myogenesis by downregulating myogenic differentiation (MyoD) and myogenin (MyoG), preserved undifferentiated reserve cell pools by upregulating myogenic factor 5 (Myf5) and retinoblastoma-like protein p130 (p130), and enhanced energy reserves by decreasing intracellular reactive oxygen species (ROS) and enhancing mitochondrial membrane potential, mitochondrial mass, and ATP content. The effect of cordycepin on myogenesis was associated with increased phosphorylation of extracellular signal-regulated kinase 1/2 (p-ERK1/2). PD98059 (a specific inhibitor of p-ERK1/2) attenuated the inhibitory effect of cordycepin on C2C12 differentiation. The present study reveals that cordycepin inhibits myogenesis through ERK1/2 MAPK signalling activation accompanied by an increase in skeletal muscle energy reserves and improving skeletal muscle oxidative stress, which may have implications for its further application for the prevention and treatment of degenerative muscle diseases caused by the depletion of depleted muscle stem cells.
Topics: MAP Kinase Signaling System; Cell Differentiation; Deoxyadenosines; Muscle Development
PubMed: 37453196
DOI: 10.1016/j.biopha.2023.115163 -
Biochemical and Biophysical Research... Sep 2021Myogenesis is a complex process regulated by several factors. This study evaluated the functional interaction between vitamin C and a high dose of capsaicin (a potential...
Myogenesis is a complex process regulated by several factors. This study evaluated the functional interaction between vitamin C and a high dose of capsaicin (a potential endoplasmic reticulum (ER) stress inducer) on myogenesis. After the induction of differentiation, treatment with ascorbic acid or ascorbic acid phosphate (AsAp) alone had minimal effects on myogenesis in C2C12 cells. However, treatment with capsaicin (300 μM) in undifferentiated C2C12 cells increased the expression levels of genes related to ER stress as well as oxidative stress. Myogenesis was effectively enhanced in C2C12 cells treated with a combination of capsaicin (300 μM) for one day before differentiation stimulation and AsAp for four days post-differentiation; subsequently, thick and long myotubes formed, and the expression levels of myosin heavy chain (MYH) 1/2 and Myh1, Myh4, and Myh7 increased. Considering that mild ER stress stimulates myogenesis, AsAp may elicit myogenesis through the alleviation of oxidative stress-induced negative effects in capsaicin-pretreated cells. The enhanced expression of Myh1 and Myh4 coincided with the expression of Col1a1, a type I collagen, suggesting that the fine-tuning of the myogenic cell microenvironment is responsible for efficient myogenesis. Our results indicate that vitamin C is a potential stimulator of myogenesis in cells, depending on the cell context.
Topics: Animals; Ascorbic Acid; Capsaicin; Cell Differentiation; Cell Line; Endoplasmic Reticulum Stress; Mice; Muscle Development; Muscle Fibers, Skeletal; Myoblasts
PubMed: 34198164
DOI: 10.1016/j.bbrc.2021.06.067 -
Journal of Molecular Histology Aug 2021Tongue muscles are derived from mesodermal cells, while signals driven by cranial neural crest cells (CNCCs) regulate tongue myogenesis via tissue-tissue interaction....
Tongue muscles are derived from mesodermal cells, while signals driven by cranial neural crest cells (CNCCs) regulate tongue myogenesis via tissue-tissue interaction. Based on such mechanisms of interaction, congenital tongue defects occur in CNC-related syndromes in humans. This study utilized a pathologic model for the syndrome of congenital bony syngnathia, Wnt1-Cre;pMes-Bmp4 mouse line, to explore impacts of enhanced CNCCs-originated BMP4 signal on tongue myogenesis via tissue-tissue interaction. Our results revealed that microglossia, a clinical phenotype of congenital bony syngnathia in humans exhibited in Wnt1-Cre;pMes-Bmp4 mice due to impaired myogenesis. The augmented BMP4 signal affected the distal distribution, proliferation, and differentiation of myogenic cells as well as tendon patterning, resulting in disarrangement and atrophy of tongue muscles and the loss of the anterior digastric muscle. This study demonstrated how a CNCCs-originated ligand impaired tongue myogenesis via a non-autonomous way, which provided potential formation mechanisms for understanding tongue abnormalities in CNC-related syndromes.
Topics: Animals; Bone Morphogenetic Protein 4; Cell Differentiation; Cell Movement; Cell Proliferation; Gene Expression Regulation, Developmental; Immunohistochemistry; In Situ Hybridization; Mice; Mice, Transgenic; Muscle Development; Neural Crest; Signal Transduction; Tongue; Tongue Diseases
PubMed: 34076834
DOI: 10.1007/s10735-021-09987-9 -
Cold Spring Harbor Perspectives in... Feb 2017Development of skeletal muscle is a multistage process that includes lineage commitment of multipotent progenitor cells, differentiation and fusion of myoblasts into... (Review)
Review
Development of skeletal muscle is a multistage process that includes lineage commitment of multipotent progenitor cells, differentiation and fusion of myoblasts into multinucleated myofibers, and maturation of myofibers into distinct types. Lineage-specific transcriptional regulation lies at the core of this process, but myogenesis is also regulated by extracellular cues. Some of these cues are initiated by direct cell-cell contact between muscle precursor cells themselves or between muscle precursors and cells of other lineages. Examples of the latter include interaction of migrating neural crest cells with multipotent muscle progenitor cells, muscle interstitial cells with myoblasts, and neurons with myofibers. Among the signaling factors involved are Notch ligands and receptors, cadherins, Ig superfamily members, and Ephrins and Eph receptors. In this article we describe recent progress in this area and highlight open questions raised by the findings.
Topics: Animals; Cell Differentiation; Cell Fusion; Cell Lineage; Humans; Muscle Development; Muscle, Skeletal
PubMed: 28062562
DOI: 10.1101/cshperspect.a029298 -
FASEB Journal : Official Publication of... Dec 2016Reduced oxygen (O) levels (hypoxia) are present during embryogenesis and exposure to altitude and in pathologic conditions. During embryogenesis, myogenic progenitor... (Review)
Review
Reduced oxygen (O) levels (hypoxia) are present during embryogenesis and exposure to altitude and in pathologic conditions. During embryogenesis, myogenic progenitor cells reside in a hypoxic microenvironment, which may regulate their activity. Satellite cells are myogenic progenitor cells localized in a local environment, suggesting that the O level could affect their activity during muscle regeneration. In this review, we present the idea that O levels regulate myogenesis and muscle regeneration, we elucidate the molecular mechanisms underlying myogenesis and muscle regeneration in hypoxia and depict therapeutic strategies using changes in O levels to promote muscle regeneration. Severe hypoxia (≤1% O) appears detrimental for myogenic differentiation in vitro, whereas a 3-6% O level could promote myogenesis. Hypoxia impairs the regenerative capacity of injured muscles. Although it remains to be explored, hypoxia may contribute to the muscle damage observed in patients with pathologies associated with hypoxia (chronic obstructive pulmonary disease, and peripheral arterial disease). Hypoxia affects satellite cell activity and myogenesis through mechanisms dependent and independent of hypoxia-inducible factor-1α. Finally, hyperbaric oxygen therapy and transplantation of hypoxia-conditioned myoblasts are beneficial procedures to enhance muscle regeneration in animals. These therapies may be clinically relevant to treatment of patients with severe muscle damage.-Chaillou, T. Lanner, J. T. Regulation of myogenesis and skeletal muscle regeneration: effects of oxygen levels on satellite cell activity.
Topics: Animals; Cell Differentiation; Humans; Muscle Development; Muscle, Skeletal; Oxygen; Regeneration; Satellite Cells, Skeletal Muscle
PubMed: 27601440
DOI: 10.1096/fj.201600757R -
Seminars in Cell & Developmental Biology Aug 2015Like other subclasses within the PAX transcription factor family, PAX3 and PAX7 play important roles in the emergence of a number of different tissues during... (Review)
Review
Like other subclasses within the PAX transcription factor family, PAX3 and PAX7 play important roles in the emergence of a number of different tissues during development. PAX3 regulates neural crest and, together with its orthologue PAX7, is also expressed in parts of the central nervous system. In this chapter we will focus on their role in skeletal muscle. Both factors are key regulators of myogenesis where Pax3 plays a major role during early skeletal muscle formation in the embryo while Pax7 predominates during post-natal growth and muscle regeneration in the adult. We review the expression and functions of these factors in the myogenic context. We also discuss mechanistic aspects of PAX3/7 function and modulation of their activity by interaction with other proteins, as well as the post-transcriptional and transcriptional regulation of their expression.
Topics: Animals; Cell Differentiation; Cell Proliferation; Humans; Muscle Development; PAX3 Transcription Factor; PAX7 Transcription Factor; Paired Box Transcription Factors
PubMed: 26424495
DOI: 10.1016/j.semcdb.2015.09.017 -
Neuroscience Letters Jun 2020For the first time, a review article focuses exclusively on the role of the protein kinase CK2 in mono- and poly-nucleated mammalian skeletal muscle cells. While CK2, a... (Review)
Review
For the first time, a review article focuses exclusively on the role of the protein kinase CK2 in mono- and poly-nucleated mammalian skeletal muscle cells. While CK2, a pleiotropic serine/threonine kinase was originally thought to phosphorylate mainly casein, later evidence found glycogen phosphorylase and glycogen synthase also to be a target, linking the enzyme to muscle biology. Indeed, recent studies have shown that CK2 is involved in many different steps in the biology of striated skeletal muscle, such as myogenesis and homeostasis in the adult muscle, and even at the neuromuscular junctions, the points of contact between the muscle fibers and the motor nerves end. Next to the role of CK2 in muscle physiology, this review also highlights the contribution of CK2 in muscle pathologies, such as muscle tumors and myopathies.
Topics: Animals; Casein Kinase II; Humans; Muscle Development; Muscle Fibers, Skeletal; Muscle, Skeletal; Neuromuscular Junction; Rhabdomyosarcoma
PubMed: 32380140
DOI: 10.1016/j.neulet.2020.135001