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Satellite cells and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Neil R.W. Martin, Adam P. Sharples
Genetic depletion of satellite cells in mice before functional overload (synergist ablation surgery) or chemical muscle injury results in an increase in fibroblast numbers and excessive production of ECM proteins (7, 85). Evidence that satellite cells directly communicate with fibroblasts comes from in vitro experiments. When myoblasts are cultured in a media which is subsequently transferred to fibroblasts, collagen synthesis is reduced in the fibroblasts (85), suggesting that myoblasts secrete a product which influences fibroblast synthesis of ECM proteins. Myoblasts can also release exosomes (a type of very small extracellular vesicle), which contain a microRNA called miR-206 that is transported into fibroblasts. miR-206 specifically represses the translation of a gene called Ribosomal binding protein-1 (Rrbp-1) which is important for collagen synthesis in fibroblasts (84). The levels of miR-206 are normally increased following muscle loading, which represses Rrbp-1 and prevents excessive ECM production by fibroblasts. However, when satellite cells are absent, miR-206 cannot be synthesised or transported to fibroblasts via exosomes, and the result is excessive collagen production and fibrosis (84). Overall, it is apparent that satellite cells communicate with fibroblasts via secretory factors and exosomes to regulate the production of ECM proteins following muscle loading.
Peripheral muscles
Published in Claudio F. Donner, Nicolino Ambrosino, Roger S. Goldstein, Pulmonary Rehabilitation, 2020
Luis Puente-Maestu, François Maltais, André Nyberg, Didier Saey
In line with the observation of type I fibre atrophy, the mRNA and/or protein expression of key mitochondrial transcriptional factors and coactivators, including peroxisome proliferator-activated receptor coactivator-1 (PGC1), peroxisome proliferator-activated receptors (PPAR), and mitochondrial transcription factor A (Tfam), are also reduced; however, the acute response of PGC-1α to exercise is normal or even enhanced, as it is the response of superoxide dismutase and synthesis of mitochondrial DNA, indicating that the short-term mitochondrial biogenetic response to exercise is appropriate (2,22). In keeping with these observations, the expression of miR-1 and miR-206 (microRNAs which have key roles in the development and differentiation of skeletal muscles) were increased in the quadriceps of COPD patients with muscle weakness and wasting (26), while in other experiments, levels of miR-1 were lower in the quadriceps of COPD patients with preserved body composition (26), suggesting an increased stimulus for muscle biogenesis in those with muscle wasting.
Role of Micronutrients in Prevention of Coronary Artery Disease and Improvement of the Standard Therapy
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Table 5.2 summarizes changes in the expression of cellular microRNAs in CAD patients. Reduced expression of miR-31 leads in to the elevation of the levels of its target proteins FAT atypical cadherin 4 and thromboxane A2 receptor in the endothelial progenitor cells (EPCs) from patients with CAD.61 Overexpression of miR-31 in CAD EPCs restored their ability to participate in angiogenesis and vasculogenesis in both in vitro and in vivo. Furthermore, lower expression of miR-720 leads to increased levels of its target protein vasohibin-1 in the EPCs from patients with CAD. Thus, downregulation of miR-31 and miR-720 contribute to the pathogenesis of CAD. The expression of miR-206 was elevated and its target protein phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunitA isoform (PIK3G2-α) in EPCs from CAD patients. Deletion of miR-206 restored angiogenesis and vasculogenesis functions of EPCs.62 Elevated expression of miR-23a downregulated its target protein epidermal growth factor receptor (EGFR) in EPCs from CAD patients. Knockingdown of miR-23a restored functions of EPCs and enhanced blood flow recovery in ischemic limbs of mice.63 The expression of miR-214 was enhanced and its target protein vascular endothelial growth factor (VEGF) was reduced in EPCs from patients with CAD. Deletion of miR-214 restored normal function of EPCs.64
Mir-206 partially rescues myogenesis deficiency by inhibiting CUGBP1 accumulation in the cell models of myotonic dystrophy
Published in Neurological Research, 2019
Wei Dong, Xuanying Chen, Menghong Wang, Zeqi Zheng, Xing Zhang, Qunlin Xiao, Xiaoping Peng
A recent study revealed that the expression of the myomiR miR-206 was upregulated by SB431542, a potent ALK4/5/7 inhibitor that reduces Smad2 signaling, in differentiating C2C12 cells [34]. MyoD is one of the earliest markers of myogenic commitment, and miRNAs are an important part of the network of early myogenesis regulators[35]. Our recent research demonstrated that Celf1 is an important target that mediates the function of miR-322/-503. The miR-322/-503 cluster, which specifically regulates the cardiomyocyte and myoblast programs, is the most promising candidate of these miRNAs. However, a recent study published by Fritegotto et al. measured the levels of muscle-specific myo-miRNAs (miR-1, miR-133a/b, miR-206) in the muscle of 12 DM1 patients and revealed that miR-206 levels were significantly increased [36]. However, this result contradicts the expression of miR-206 in vitro, which may because the histopathological score was inversely correlated with disease duration and not significantly correlated with the levels of myo-miRNAs. At present, our research is still at the cellular level, and so the role of miR-206 needs to be tested further in vivo. Further studies into these miRNAs may lead to the identification of new drug candidates for treating cardiac and skeletal muscle injuries such as myocardial ischemia and muscular dystrophies.
Competing endogenous RNA networks in cervical cancer: function, mechanism and perspective
Published in Journal of Drug Targeting, 2019
The miRNA-1 is formed by miR-1-1, miR-1–2 and miR-206. miR-206 is found in chromosome 6 and miR-1–1 and miR-1–2 are localised in chromosome 20 and 18, respectively. miR-1–1 and miR-1–2 originate the same mature sequence. Hu et al. [53] proved that miR-1 levels correlate negatively with the clinicopathologic features in HR-HPV 16/18-infected cervical cancer patients. MiR-1 overexpression inhibited proliferation and promoted apoptosis in cervical cancer cells and reduced xenograft tumour growth in nude mice. Mechanically, they demonstrated that miR-1 was associated with AGO proteins by targeting ectopic glucose-6-phosphate dehydrogenase (G6PD) in high risk HPV-infected human cervical cancer cells.
Circulating miRNAs as biomarkers for early diagnosis of coronary artery disease
Published in Expert Opinion on Therapeutic Patents, 2018
Lei Zhang, Yuan Zhang, Yanfang Zhao, Yu Wang, Han Ding, Sheng Xue, Peifeng Li
Apart from the miRNAs related to atherosclerosis, some other miRNAs also involve in CAD formation or inhibition. The dysfunction of cardiac muscle can lead to CAD. Cardiac muscle-enriched microRNAs consist of several miRNAs, such as miR-1, miR-133a, miR-208a, miR-208b, and miR-499. MiR-1, miR-133a, and miR-208a were found to be higher in patients with CAD [41,58,87,104], while miR-208b was reported to be increased in the plasma of CAD patients. MiR-206 and miR-574-5p have been found to be associated with cardiovascular diseases [127–129]. The circulation levels of these two miRNAs were much higher in CAD patients in comparison with the healthy controls [130]. Serum miR-130a was increased in the sclerotic samples [75]. MiR-135a was found to increase in PBMCs of CAD [95]. Circulating expression patterns of miR-451 and the miR-106b/25 cluster were upregulated in vulnerable CAD [76]. Circulating level of miR-125a, miR-486, miR-197, miR-1229, miR-134, miR-3135b, miR-2861, miR-199a, miR-337-5p, miR-433, and miR-485-3p were all increased in CAD patients [41,63,84,87,131]. In a report regarding CAD in middle-aged (40–60 years old) patients, plasma level of miR-765 was higher, whereas plasma miR-149 and miR-424 were lower in CAD patients than in normal people [43,44]. Weber et al. carried out experiments with whole blood and they discovered that miR-19a, miR-29a, miR-30e-5p, miR-150, miR-181d, miR-342, miR-378, and miR-584 were notably downregulated in the blood of CAD patients [124]. Du et al. reviewed that miR-196-5p, miR-190a-5p, and miR-3163-3p exhibited decreased expression in the serum of CAD patients compared with control subjects [77]. The reduced expression of circulating miR-199a was also reported in Jansen’s work [80]. Some other miRNAs, such as miR-181a and miR-16, showed lower circulating level in CAD patients [120].