scholarly journals Amla Enhances Mitochondrial Spare Respiratory Capacity by Increasing Mitochondrial Biogenesis and Antioxidant Systems in a Murine Skeletal Muscle Cell Line

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hirotaka Yamamoto ◽  
Katsutaro Morino ◽  
Lemecha Mengistu ◽  
Taishi Ishibashi ◽  
Kohei Kiriyama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Cell ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Skeletal Muscle Cell ◽  
Antioxidant Systems ◽  
Respiratory Capacity ◽  
Age Related ◽  
Murine Skeletal Muscle

Amla is one of the most important plants in Indian traditional medicine and has been shown to improve various age-related disorders while decreasing oxidative stress. Mitochondrial dysfunction is a proposed cause of aging through elevated oxidative stress. In this study, we investigated the effects of Amla on mitochondrial function in C2C12 myotubes, a murine skeletal muscle cell model with abundant mitochondria. Based on cell flux analysis, treatment with an extract of Amla fruit enhanced mitochondrial spare respiratory capacity, which enables cells to overcome various stresses. To further explore the mechanisms underlying these effects on mitochondrial function, we analyzed mitochondrial biogenesis and antioxidant systems, both proposed regulators of mitochondrial spare respiratory capacity. We found that Amla treatment stimulated both systems accompanied by AMPK and Nrf2 activation. Furthermore, we found that Amla treatment exhibited cytoprotective effects and lowered reactive oxygen species (ROS) levels in cells subjected to t-BHP-induced oxidative stress. These effects were accompanied by increased oxygen consumption, suggesting that Amla protected cells against oxidative stress by using enhanced spare respiratory capacity to produce more energy. Thus we identified protective effects of Amla, involving activation of mitochondrial function, which potentially explain its various effects on age-related disorders.

Activation by curare of acetylcholine receptor channels in a murine skeletal muscle cell line

1989 ◽  
Vol 67 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Catherine E. Morris ◽  
Madeleine R. Montpetit ◽  
Wade J. Sigurdson ◽  
Kuni Iwasa
Keyword(s):  
Skeletal Muscle ◽  
Cell Line ◽  
Acetylcholine Receptor ◽  
Muscle Cell ◽  
Skeletal Muscle Cell ◽  
Single Channels ◽  
Agonist Action ◽  
Murine Skeletal Muscle ◽  
Skeletal Muscle Cell Line ◽  
Muscle Cell Line

Curare action on nicotinic acetylcholine receptors has a number of facets, of which the best known is competitive antagonism. Here we describe the weak agonist action of 10−5 M curare on the murine skeletal muscle cell line, G8. Although curare induces no depolarization in G8 cells, single-channel recordings reveal short-lived curare-induced currents. A feature of these brief events is the multiplicity of conductance levels (of the four levels with conductances of 48, 37, 14, and 6 pS, none had a lifetime greater than 1.5 ms). Most well-resolved events (about 17% of which are to a subconductance) last less than 0.5 ms, with activation occurring predominantly as isolated events rather than in bursts. Agonism is not, however, a high probability action for curare: calculations based on the frequency of events at half-saturating conditions suggest that curare-induced channel openings occur during less than 1% of acetylcholine receptor – curare binding episodes. The outcome is (a) an agonist action too feeble to perturb the membrane voltage and (b) a powerful competitive antagonist action.Key words: curare, acetylcholine receptor, single channels, skeletal muscle.

Blueberry fruit polyphenolics suppress oxidative stress-induced skeletal muscle cell damagein vitro

2010 ◽  
Vol 54 (3) ◽  
pp. 353-363 ◽  
Author(s):  
Roger D. Hurst ◽  
Robyn W. Wells ◽  
Suzanne M. Hurst ◽  
Tony K. McGhie ◽  
Janine M. Cooney ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Cell ◽  
Skeletal Muscle Cell

Skeletal Muscle Cell Oxidative Stress as a Possible Therapeutic Target in a Denervation-Induced Experimental Sarcopenic Model

Spine ◽  
2019 ◽  
Vol 44 (8) ◽  
pp. E446-E455 ◽  
Author(s):  
Hideyuki Kinoshita ◽  
Sumihisa Orita ◽  
Kazuhide Inage ◽  
Kazuyo Yamauchi ◽  
Koki Abe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Cell ◽  
Therapeutic Target ◽  
Skeletal Muscle Cell

PGC-1α-mediated regulation of mitochondrial function and physiological implications

2020 ◽  
Vol 45 (9) ◽  
pp. 927-936
Author(s):  
Jens Frey Halling ◽  
Henriette Pilegaard
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Current Evidence ◽  
Peroxisome Proliferator ◽  
Control Mechanisms ◽  
Peroxisome Proliferator Activated Receptor ◽  
Age Related ◽  
Mitochondrial Functions

The majority of human energy metabolism occurs in skeletal muscle mitochondria emphasizing the importance of understanding the regulation of myocellular mitochondrial function. The transcriptional co-activator peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) has been characterized as a major factor in the transcriptional control of several mitochondrial components. Thus, PGC-1α is often described as a master regulator of mitochondrial biogenesis as well as a central player in regulating the antioxidant defense. However, accumulating evidence suggests that PGC-1α is also involved in the complex regulation of mitochondrial quality beyond biogenesis, which includes mitochondrial network dynamics and autophagic removal of damaged mitochondria. In addition, mitochondrial reactive oxygen species production has been suggested to regulate skeletal muscle insulin sensitivity, which may also be influenced by PGC-1α. This review aims to highlight the current evidence for PGC-1α-mediated regulation of skeletal muscle mitochondrial function beyond the effects on mitochondrial biogenesis as well as the potential PGC-1α-related impact on insulin-stimulated glucose uptake in skeletal muscle. Novelty PGC-1α regulates mitochondrial biogenesis but also has effects on mitochondrial functions beyond biogenesis. Mitochondrial quality control mechanisms, including fission, fusion, and mitophagy, are regulated by PGC-1α. PGC-1α-mediated regulation of mitochondrial quality may affect age-related mitochondrial dysfunction and insulin sensitivity.

scholarly journals Conditionally Immortalised Equine Skeletal Muscle Cell Lines for in Vitro Analysis

2021 ◽  
Author(s):  
Mary Francis Rooney ◽  
Nuno Neto ◽  
Michael Monaghan ◽  
Emmeline Hill ◽  
Richard Porter
Keyword(s):  
Skeletal Muscle ◽  
Cell Lines ◽  
Muscle Cell ◽  
Mitochondrial Function ◽  
Ex Vivo ◽  
Skeletal Muscle Cell ◽  
Cell Phenotype ◽  
Metabolic Function ◽  
Thoroughbred Horse

Abstract BackgroundThoroughbred racehorse performance is largely influenced by a major quantitative trait locus at the myostatin (MSTN) gene which determines aptitude for certain race distances due to a promoter region insertion mutation influencing functional phenotypes in skeletal muscle. To develop an in vitro system for functional experiments we established three novel equine skeletal muscle cell lines reflecting the variation in phenotype associated with MSTN genotype (CC/II, CT/IN and TT/NN for SNP g.66493737C>T/SINE insertion 227 bp polymorphism). Primary equine skeletal muscle myoblasts, isolated from Thoroughbred horse gluteus medius, were conditionally immortalised and evaluated to determine whether cell phenotype and metabolic function were comparable to functional characteristics previously reported for ex vivo skeletal muscle isolated from Thoroughbred horses with each genotype.ResultsPrimary myoblasts conditionally immortalized with the temperature sensitive SV40TtsA58 lentivirus vector successfully proliferated and could revert to their primary cell phenotype and differentiate into multinucleated myotubes. Skeletal muscle fibre type, MSTN gene expression, mitochondrial abundance, and mitochondrial function of the three MSTN genotype cell lines, were consistent with equivalent characterisation of ex vivo skeletal muscle samples with these genotypes. Furthermore, addition of coenzyme Q10 (CoQ10) to the cell lines improved mitochondrial function, an observation consistent with ex vivo skeletal muscle samples with these genotypes following supplementation with CoQ10 in the diet. ConclusionsThe observation that the phenotypic characteristics and metabolic function of the cells lines are equivalent to ex vivo skeletal muscle indicates that this in vitro system will enable efficient and cost-effective analyses of equine skeletal muscle for a range of different applications including understanding metabolic function, testing of nutritional supplements, drug test development and gene doping test development. In the multi-billion-euro international Thoroughbred horse industry research advances in the biological function of skeletal muscle are likely to have considerable impact. Furthermore, this novel genotype-specific system may be adapted and applied to human biomedicine to improve understanding of the effects of myostatin in human physiology and medicine.

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