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Strategies for Elucidating Immunological Mechanisms in Intestinal Smooth Muscle Pathophysiology
Published in William J. Snape, Stephen M. Collins, Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves, 2020
However, recent studies of commitment of stem cells to the myoid lineage, and of growth factors in myogenic differentiation demonstrate novel and important directions for future research. In the commitment of fibroblast-like mesenchymal cells to the myoid lineage, expression of the protein Myf-5 can induce the myogenic phenotype in embryonic “fibroblasts”.17 This protein seems to part of a family of genes potentially involved in myogenic differentiation and in the ability of the cells to form multinucleated syncytia and myosin heavy chains.
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
Protein and amino acids
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
As mentioned previously, NPB is a result of MPS and MPB. During resistance training, the goal is to increase MPS with as little effect on MPB as possible. The resulting protein accretion can lead to increases in muscle mass and strength over the course of resistance training. Since many tissues other than muscle also undergo synthesis and breakdown, this leads to the issue of whole-body protein turnover and can be increased due to catabolically-related conditions such as hypocalorism and exercise inflammation. However, it is common that ongoing high-intensity exercise (either aerobic or resistance exercise) in conjunction with inadequate daily calories will augment MPB so that the liberated amino acids can be used as a fuel source. As a result, these conditions are associated with physiological, and perhaps psychological, stress and cause an increase in the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Inevitably this results in a release of cortisol from the cortical area of the adrenal gland into circulation. Cortisol is a lipophilic hormone and in muscle will diffuse across the sarcolemma where it can bind with the intracellular glucocorticoid receptor (GR). Once bound, the GR becomes an activated transcription factor with DNA binding properties and will translocate into the nucleus where it will bind enhancer elements in the regulatory promoter region within various proteolytic genes such as those associated with the ATP-dependent ubiquitin proteolytic pathway (Atrogin-1, MuRF-1 FoxO, ubiquitin) and myostatin (83). Conversely, the expression of various genes associated with up-regulating muscle hypertrophic processes, such as the myogenic regulatory factors (MyoD, myogenin, MRF4 and MYF5), are down-regulated. The overall catabolic process involving muscle proteolysis ultimately results in MPB and a subsequent release of amino acids into circulation. As previously mentioned, the goal during exercise training (especially resistance training) is to minimize this process as much as possible, which can be accomplished with proper post-exercise recovery practices, including adequate daily intake of protein and total calories.
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.
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
To determine whether genistein also has a bidirectional regulation effect on C2C12 myoblast differentiation, we treated differentiating cells with the same treatment concentrations on the proliferating cells. Interestingly, we again found a bidirectional regulation in the myoblast differentiation. Similar to our results, Hinard et al. (2008) found that 10 µM/L genistein accelerated myoblast fusion (up to 28%, control: 6%), and Woo et al. (2006) reported that 20 µM/L genistein inhibited myoblast fusion. We also found a decreasing trend in myotube diameter with increasing treatment concentrations of genistein. However, the cause of this phenomenon needs further exploration in future studies. The determination and differentiation of muscle cells are governed by four key transcription factors: MyoG, MyoD, Myf5, and MRF4. MyoD and Myf5 are identified as determinants of myogenesis, whereas MyoG and MRF4 are highly expressed during terminal differentiation and trigger myoblasts to fuse to form myotubes (Berkes & Tapscott 2005; Montarras et al., 1991). Our data indicate that MyoG, MyoD, and MRF4 were up-regulated at 10 µM/L genistein, but MyoG, MyoD, and Myf5 were down-regulated at 100 µM/L genistein. This is consistent with previous observations that MyoG and MyoD expression increased with genistein treatment in mice (diet, genistein <10 µg/g) and rats (Velders et al., 2012; Zhou & Liu, 2013). Genistein is widely used in biomedical field as a broad-spectrum tyrosine kinase (TK) inhibitor. Our results showed the inhibitory effect of 100 µM/L genistein on IGF-1R, a typical RTK, yet the lower concentration have no effect, which consistent with previous reports (Hwang et al., 2013).
Trimetazidine ameliorates hindlimb ischaemic damage in type 2 diabetic mice
Published in Annals of Medicine, 2021
Yan Yang, Qinqin Xu, Tao Li, Shiying Shao
We further detected the expression of myogenin and Myf5, two myogenic markers. The result indicated an obvious decrease of myogenin in PAD model (0.22 ± 0.08 vs. control group, p < .05) while administration of TMZ significantly increased myogenin expression in the ischaemic hindlimb of diabetic mice. We also detected the decreased expression of Myf5, which could be corrected by TMZ administration (TMZ group 0.66 ± 0.14 vs. saline group 0.12 ± 0.06, p < .01) (Figure 5(A,B)). Collectively, these results indicate that TMZ have the potential to enhance the regeneration of ischaemic muscles in diabetic mice through myogenic regulation pathway.