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Signal transduction and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Brendan Egan, Adam P. Sharples
The proximal promoter is a region of DNA up to a few hundred base pairs upstream from the core promoter, whereas enhancer regions can often be hundreds of thousands of base pairs away from the transcription start site. Loops in the DNA bring distal enhancer regions close to the proximal promoter. Indeed, it is very rare for an enhancer to affect genes that are adjacent to it in the DNA sequence. Current predictions suggest that there are ~70,000 regions with promoter-like features and ~400,000 regions with enhancer-like features in the human genome (53), which gives an indication of the complexity of this process. To give an example from skeletal muscle, the myogenic regulatory factor MyoD binds to >20,000 DNA sites in muscle cells (54).
Exercise, Metabolism and Oxidative Stress in the Epigenetic Landscape
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Gareth W. Davison, Colum P. Walsh
In a skeletal muscle context, ACLY silencing impairs myoblast and satellite cell differentiation, accompanied by a decrease in the gene expression of fast myosin heavy chain isoforms, and the myogenic regulatory factor MyoD. Conversely, overexpression of ACLY enhances MyoD expression via hyperacetylation of H3K9, 14 and 27 (Das et al., 2017). In this regard, it is theoretically plausible that exercise stress may stimulate the pathway involving ACYL induction and the conversion of citrate to acetyl-CoA. This metabolic flux may lead to hyperacetylation of key skeletal muscle remodelling transcripts (Seaborne and Sharples, 2020). Using a whole-genome sequencing approach, Sailani et al. (2019) determined that lifelong exercise can positively modify the epigenome to protect skeletal muscle cells against a reduced metabolic capacity and oxidative stress. DNA methylation was differentially lower (in exercise vs sedentary) in 714 promoters for genes encoding critical enzymes relating to glycogen metabolism, glycolysis, and the TCA cycle. In general, promoter regions of genes involved in the oxidative stress response were hypomethylated in the exercise group. Collectively, these hypomethylation profiles suggest that lifelong exercise can manipulate the capacity for glycolysis and TCA cycle flux and protect cells from age-related damage and deterioration brought on by oxidative stress.
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.
Common therapeutic advances for Duchenne muscular dystrophy (DMD)
Published in International Journal of Neuroscience, 2021
Arash Salmaninejad, Yousef Jafari Abarghan, Saeed Bozorg Qomi, Hadi Bayat, Meysam Yousefi, Sara Azhdari, Samaneh Talebi, Majid Mojarrad
Skeletal muscle stem cells, also called Satellite Cells (SCs), are the adult muscle stem cells which reside at the sarcolemma and the basal lamina of the muscle fibre is among initial stem cells that can be used for cell-based therapy. After muscle injury, SCs divide and give rise to SC progeny (the myoblasts) that regenerate or substitute the damaged fibres. The differentiation process of stimulated SCs toward myogenic is managed by myogenic regulatory factors (MRFs), comprising MRF4, Myf5, myogenin, MyoD and epigenetic element [193,194]. Moreover, it was indicated that the transcription factor Pax7 is a master transcriptional regulator and also it is critical for proliferation and cell cycle progression of SCs and myoblasts [195]. Likewise, chromatin-modifying enzymes control gene expression programs in myotubes, myoblasts, and SCs. It was shown that muscle differentiation is developed when the cells treated with histone deacetylase inhibitors (HDAC) and as a consequence, the muscular dystrophy phenotype ameliorated (Figure 1f) [196].
Bidirectional regulation of genistein on the proliferation and differentiation of C2C12 myoblasts
Published in Xenobiotica, 2020
Mailin Gan, Dongli Yang, Yuan Fan, Jingjing Du, Linyuan Shen, Qiang Li, Yanzhi Jiang, Guoqing Tang, Mingzhou Li, Jinyong Wang, Xuewei Li, Shunhua Zhang, Li Zhu
C2C12 myoblast differentiation was promoted with the treatment of 10 µM/L genistein (p < 0.05), but it was inhibited at 20–100 µM/L genistein (p < 0.01) (Figure 2A and B). Except for 50 µM/L (p < 0.05), genistein had no significant effects on myotube length and diameter, and the 100 µM/L group had no observed myotubes (Figure 2C). The expression levels of the muscle-specific gene, myosin heavy chain (MyHC), demonstrated a trend similar to that of the myotube fusion index (Figure 2D). Furthermore, the expression levels of myogenic factors MyoG (myogenin), MyoD (myogenic differentiation antigen), and MRF4 (myogenic regulatory factor 4) were increased at the concentration that demonstrated a significant change in MyHC (10 µM/L; p < 0.01). However, MyoG, MyoD, and Myf5 (myogenic factor 5) were decreased after treatment with 100 µM/L genistein (p < 0.01) (Figure 2E). The expression of ERα (estrogen receptor-α), which is the binding substrate of genistein was increased after treatment with 10 µM/L genistein (p < 0.05), but ERα and IGF-1R (insulin-like growth factor 1 receptor), a typical receptor tyrosine kinase (RTK) were both decreased in 100 µM/L genistein (p < 0.01) (Figure 2F).