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muscular protein synthesis

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https://www.readbyqxmd.com/read/27874066/cl316-243-a-%C3%AE-3-adrenergic-receptor-agonist-induces-muscle-hypertrophy-and-increased-strength
#1
Daniela Puzzo, Roberto Raiteri, Clotilde Castaldo, Raffaele Capasso, Ester Pagano, Mariateresa Tedesco, Walter Gulisano, Lisaveta Drozd, Pellegrino Lippiello, Agostino Palmeri, Pietro Scotto, Maria Concetta Miniaci
Studies in vitro have demonstrated that β3-adrenergic receptors (β3-ARs) regulate protein metabolism in skeletal muscle by promoting protein synthesis and inhibiting protein degradation. In this study, we evaluated whether activation of β3-ARs by the selective agonist CL316,243 modifies the functional and structural properties of skeletal muscles of healthy mice. Daily injections of CL316,243 for 15 days resulted in a significant improvement in muscle force production, assessed by grip strength and weight tests, and an increased myofiber cross-sectional area, indicative of muscle hypertrophy...
November 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27866827/nucleoprotein-supplementation-enhances-the-recovery-of-rat-soleus-mass-with-reloading-after-hindlimb-unloading-induced-atrophy-via-myonuclei-accretion-and-increased-protein-synthesis
#2
Ryosuke Nakanishi, Yusuke Hirayama, Minoru Tanaka, Noriaki Maeshige, Hiroyo Kondo, Akihiko Ishihara, Roland R Roy, Hidemi Fujino
Hindlimb unloading results in muscle atrophy and a period of reloading has been shown to partially recover the lost muscle mass. Two of the mechanisms involved in this recovery of muscle mass are the activation of protein synthesis pathways and an increase in myonuclei number. The additional myonuclei are provided by satellite cells that are activated by the mechanical stress associated with the reloading of the muscles and eventually incorporated into the muscle fibers. Amino acid supplementation with exercise also can increase skeletal muscle mass through enhancement of protein synthesis and nucleotide supplements can promote cell cycle activity...
October 23, 2016: Nutrition Research
https://www.readbyqxmd.com/read/27845387/adenoviral-vectors-encoding-crispr-cas9-multiplexes-rescue-dystrophin-synthesis-in-unselected-populations-of-dmd-muscle-cells
#3
Ignazio Maggio, Jin Liu, Josephine M Janssen, Xiaoyu Chen, Manuel A F V Gonçalves
Mutations disrupting the reading frame of the ~2.4 Mb dystrophin-encoding DMD gene cause a fatal X-linked muscle-wasting disorder called Duchenne muscular dystrophy (DMD). Genome editing based on paired RNA-guided nucleases (RGNs) from CRISPR/Cas9 systems has been proposed for permanently repairing faulty DMD loci. However, such multiplexing strategies require the development and testing of delivery systems capable of introducing the various gene editing tools into target cells. Here, we investigated the suitability of adenoviral vectors (AdVs) for multiplexed DMD editing by packaging in single vector particles expression units encoding the Streptococcus pyogenes Cas9 nuclease and sequence-specific gRNA pairs...
November 15, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27832095/increased-muscular-5%C3%AE-dihydrotestosterone-in-response-to-resistance-training-relates-to-skeletal-muscle-mass-and-glucose-metabolism-in-type-2-diabetic-rats
#4
Naoki Horii, Koji Sato, Noboru Mesaki, Motoyuki Iemitsu
Regular resistance exercise induces skeletal muscle hypertrophy and improvement of glycemic control in type 2 diabetes patients. Administration of dehydroepiandrosterone (DHEA), a sex steroid hormone precursor, increases 5α-dihydrotestosterone (DHT) synthesis and is associated with improvements in fasting blood glucose level and skeletal muscle hypertrophy. Therefore, the aim of this study was to investigate whether increase in muscle DHT levels, induced by chronic resistance exercise, can contribute to skeletal muscle hypertrophy and concomitant improvement of muscular glucose metabolism in type 2 diabetic rats...
2016: PloS One
https://www.readbyqxmd.com/read/27798264/nad-repletion-improves-muscle-function-in-muscular-dystrophy-and-counters-global-parylation
#5
Dongryeol Ryu, Hongbo Zhang, Eduardo R Ropelle, Vincenzo Sorrentino, Davi A G Mázala, Laurent Mouchiroud, Philip L Marshall, Matthew D Campbell, Amir Safi Ali, Gary M Knowels, Stéphanie Bellemin, Shama R Iyer, Xu Wang, Karim Gariani, Anthony A Sauve, Carles Cantó, Kevin E Conley, Ludivine Walter, Richard M Lovering, Eva R Chin, Bernard J Jasmin, David J Marcinek, Keir J Menzies, Johan Auwerx
Neuromuscular diseases are often caused by inherited mutations that lead to progressive skeletal muscle weakness and degeneration. In diverse populations of normal healthy mice, we observed correlations between the abundance of mRNA transcripts related to mitochondrial biogenesis, the dystrophin-sarcoglycan complex, and nicotinamide adenine dinucleotide (NAD(+)) synthesis, consistent with a potential role for the essential cofactor NAD(+) in protecting muscle from metabolic and structural degeneration. Furthermore, the skeletal muscle transcriptomes of patients with Duchene's muscular dystrophy (DMD) and other muscle diseases were enriched for various poly[adenosine 5'-diphosphate (ADP)-ribose] polymerases (PARPs) and for nicotinamide N-methyltransferase (NNMT), enzymes that are major consumers of NAD(+) and are involved in pleiotropic events, including inflammation...
October 19, 2016: Science Translational Medicine
https://www.readbyqxmd.com/read/27798095/myeloid-cells-are-capable-of-synthesizing-aldosterone-to-exacerbate-damage-in-muscular-dystrophy
#6
Jessica A Chadwick, Sarah A Swager, Jeovanna Lowe, Steven S Welc, James G Tidball, Celso E Gomez-Sanchez, Elise P Gomez-Sanchez, Jill A Rafael-Fortney
FDA-approved mineralocorticoid receptor (MR) antagonists are used to treat heart failure. We have recently demonstrated efficacy of MR antagonists for skeletal muscles in addition to heart in Duchenne muscular dystrophy mouse models and that mineralocorticoid receptors are present and functional in skeletal muscles. The goal of this study was to elucidate the underlying mechanisms of MR antagonist efficacy on dystrophic skeletal muscles. We demonstrate for the first time that infiltrating myeloid cells clustered in damaged areas of dystrophic skeletal muscles have the capacity to produce the natural ligand of MR, aldosterone, which in excess is known to exacerbate tissue damage...
October 23, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27742803/skeletal-muscle-and-resistance-exercise-training-the-role-of-protein-synthesis-in-recovery-and-remodelling
#7
Chris McGlory, Michaela C Devries, Stuart M Phillips
Exercise results in the rapid remodelling of skeletal muscle imparting a positive impact on human health. This process is underpinned by acute and chronic changes in both gene and protein synthesis. In this short review we provide a brief summary of our current understanding regarding how exercise influences these processes as well as the subsequent impact on muscle protein turnover and resultant shift in muscle phenotype. We explore concepts of ribosomal biogenesis and the potential role of increased translational capacity versus translational efficiency in contributing to muscular hypertrophy...
October 14, 2016: Journal of Applied Physiology
https://www.readbyqxmd.com/read/27733450/new-function-of-the-myostatin-activin-type-i-receptor-alk4-as-a-mediator-of-muscle-atrophy-and-muscle-regeneration
#8
Svitlana Pasteuning-Vuhman, Johanna Boertje-van der Meulen, Maaike van Putten, Maurice Overzier, Peter Ten Dijke, Szymon M Kiełbasa, Wibowo Arindrarto, Ron Wolterbeek, Ksenia V Lezhnina, Ivan V Ozerov, Aleksandr M Aliper, Willem M Hoogaars, Annemieke Aartsma-Rus, Cindy J M Loomans
Skeletal muscle fibrosis and impaired muscle regeneration are major contributors to muscle wasting in Duchenne muscular dystrophy (DMD). Muscle growth is negatively regulated by myostatin (MSTN) and activins. Blockage of these pathways may improve muscle quality and function in DMD. Antisense oligonucleotides (AONs) were designed specifically to block the function of ALK4, a key receptor for the MSTN/activin pathway in skeletal muscle. AON-induced exon skipping resulted in specific Alk4 down-regulation, inhibition of MSTN activity, and increased myoblast differentiation in vitro Unexpectedly, a marked decrease in muscle mass (10%) was found after Alk4 AON treatment in mdx mice...
October 12, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27665016/effect-of-white-striping-myopathy-on-breast-muscle-pectoralis-major-protein-turnover-and-gene-expression-in-broilers
#9
Karen Vignale, Justina V Caldas, Judy A England, Nirun Boonsinchai, Andrew Magnuson, Erik D Pollock, Sami Dridi, Casey M Owens, Craig N Coon
A study was conducted to evaluate the effect of white striping ( WS: ) of broiler breast muscle (Pectoralis major) on protein turnover and gene expression of genes related to protein degradation and fatty acid synthesis. A total of 560 day-old male broiler chicks Cobb 500 were allocated in a total of 16 pens, 35 chicks per pen. A completely randomized design was conducted with a 2 × 3 factorial arrangement (2 scores: severe and normal, and 3 breast meat samples sites). At d 60, 20 birds were randomly selected, euthanized, and scored for white striping...
September 24, 2016: Poultry Science
https://www.readbyqxmd.com/read/27631878/mitochondrial-chchd-containing-proteins-physiologic-functions-and-link-with-neurodegenerative-diseases
#10
Zhi-Dong Zhou, Wuan-Ting Saw, Eng-King Tan
The coiled-coil-helix-coiled-coil-helix domain (CHCHD)-containing proteins are evolutionarily conserved nucleus-encoded small mitochondrial proteins with important functions. So far, nine members have been identified in this protein family. All CHCHD proteins have at least one functional coiled-coil-helix-coiled-coil-helix (CHCH) domain, which is stabilized by two pairs of disulfide bonds between two helices. CHCHD proteins have various important pathophysiological roles in mitochondria and other key cellular processes...
September 8, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27612288/digital-droplet-pcr-for-the-absolute-quantification-of-exon-skipping-induced-by-antisense-oligonucleotides-in-pre-clinical-development-for-duchenne-muscular-dystrophy
#11
Ruurd C Verheul, Judith C T van Deutekom, Nicole A Datson
Antisense oligonucleotides (AONs) in clinical development for Duchenne muscular dystrophy (DMD) aim to induce skipping of a specific exon of the dystrophin transcript during pre-mRNA splicing. This results in restoration of the open reading frame and consequently synthesis of a dystrophin protein with a shorter yet functional central rod domain. To monitor the molecular therapeutic effect of exon skip-inducing AONs in clinical studies, accurate quantification of pre- and post-treatment exon skip levels is required...
2016: PloS One
https://www.readbyqxmd.com/read/27611888/levels-of-inflammation-and-oxidative-stress-and-a-role-for-taurine-in-dystropathology-of-the-golden-retriever-muscular-dystrophy-dog-model-for-duchenne-muscular-dystrophy
#12
Jessica R Terrill, Marisa N Duong, Rufus Turner, Caroline Le Guiner, Amber Boyatzis, Anthony J Kettle, Miranda D Grounds, Peter G Arthur
Duchenne Muscular Dystrophy (DMD) is a fatal skeletal muscle wasting disease presenting with excessive myofibre necrosis and increased inflammation and oxidative stress. In the mdx mouse model of DMD, homeostasis of the amino acid taurine is altered, and taurine administration drastically decreases muscle necrosis, dystropathology, inflammation and protein thiol oxidation. Since the severe pathology of the Golden Retriever Muscular Dystrophy (GRMD) dog model more closely resembles the human DMD condition, we aimed to assess the generation of oxidants by inflammatory cells and taurine metabolism in this species...
August 30, 2016: Redox Biology
https://www.readbyqxmd.com/read/27514098/-metabolic-changes-of-skeletal-muscles-in-traumatic-injury-of-peripheral-nerve-and-autoplasty-in-experiment
#13
V V Gayovych, A M Magomedov, O M Makarenko, S I Savohsko
The changes in metabolism of the amine acids, enzymes, electrolytes, fat acids (FA) in skeletal muscles of anterior and posterior extremities of rats in significant defects of peripheral nerve and its autoplasty were studied in experimental investigation. Metabolic changes in skeletal muscles are accompanied by significant intensity of proteolysis, lowering of the enzymes activity, energetic metabolism and in a less extent of the electrolytes balance and the FA metabolism. After autoplasty of big defects in the traumatized nerve the proteins' synthesis and restoration of activity of lactate dehydrogenase and creatine phosphokinase constitute the markers of muscular tissue restoration...
March 2016: Klinichna Khirurhiia
https://www.readbyqxmd.com/read/27493216/carbohydrate-binding-domain-of-the-pomgnt1-stem-region-modulates-o-mannosylation-sites-of-%C3%AE-dystroglycan
#14
Naoyuki Kuwabara, Hiroshi Manya, Takeyuki Yamada, Hiroaki Tateno, Motoi Kanagawa, Kazuhiro Kobayashi, Keiko Akasaka-Manya, Yuriko Hirose, Mamoru Mizuno, Mitsunori Ikeguchi, Tatsushi Toda, Jun Hirabayashi, Toshiya Senda, Tamao Endo, Ryuichi Kato
The dystrophin glycoprotein complex, which connects the cell membrane to the basement membrane, is essential for a variety of biological events, including maintenance of muscle integrity. An O-mannose-type GalNAc-β1,3-GlcNAc-β1,4-(phosphate-6)-Man structure of α-dystroglycan (α-DG), a subunit of the complex that is anchored to the cell membrane, interacts directly with laminin in the basement membrane. Reduced glycosylation of α-DG is linked to some types of inherited muscular dystrophy; consistent with this relationship, many disease-related mutations have been detected in genes involved in O-mannosyl glycan synthesis...
August 16, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27276190/a-rare-form-of-limb-girdle-muscular-dystrophy-type-2e-seen-in-an-iranian-family-detected-by-autozygosity-mapping
#15
Marzieh Mojbafan, Yalda Nilipour, Seyed Hasan Tonekaboni, Samira Dabbagh Bagheri, Hamideh Bagherian, Zohreh Sharifi, Zahra Zeinali, Javad Tavakkoly-Bazzaz, Sirous Zeinali
Sarcoglycanopathies (SGPs) constitute a subgroup of autosomal recessive limb girdle muscular dystrophies (LGMDs) which are caused by mutations in sarcoglycan (SGs) genes. SG proteins form a core complex consisting of α, β, γ and δ sarcoglycans which are encoded by SGCA, SGCB, SGCG and SGCD genes, respectively. Genetic defect, in any of these SG proteins, results in instability of the whole complex. This effect can be helpful in interpreting muscle biopsy results. Autozygosity mapping is a gene mapping approach which can be applied in large consanguineous families for tracking the defective gene in most autosomal recessive disorders...
March 2016: Journal of Neurogenetics
https://www.readbyqxmd.com/read/27274754/effect-of-electroacupuncture-on-the-expression-of-glycyl-trna-synthetase-and-ultrastructure-changes-in-atrophied-rat-peroneus-longus-muscle-induced-by-sciatic-nerve-injection-injury
#16
Meng Wang, Xiao Ming Zhang, Sheng Bo Yang
Glycyl-tRNA synthetase (GlyRS) is one of the key enzymes involved in protein synthesis. Its mutations have been reported to cause Charcot-Marie-Tooth disease which demonstrates muscular atrophy in distal extremities, particularly manifested in peroneus muscles. In this situation, the dysfunctions of mitochondria and sarcoplasmic reticulum (SR) affect energy supply and excitation-contraction coupling of muscle fibers, therefore resulting in muscular atrophy. Although the treatment of muscular atrophy is a global urgent problem, it can be improved by electroacupuncture (EA) treatment...
2016: Evidence-based Complementary and Alternative Medicine: ECAM
https://www.readbyqxmd.com/read/27274715/the-effects-of-phosphatidic-acid-supplementation-on-strength-body-composition-muscular-endurance-power-agility-and-vertical-jump-in-resistance-trained-men
#17
Guillermo Escalante, Michelle Alencar, Bryan Haddock, Phillip Harvey
BACKGROUND: Phosphatidic acid (PA) is a lipid messenger that has been shown to increase muscle protein synthesis via signaling stimulation of the mammalian target of rapamycin (mTOR). MaxxTOR® (MT) is a supplement that contains PA as the main active ingredient but also contains other synergistic mTOR signaling substances including L-Leucine, Beta-Hydroxy-Beta-Methylbutyrate (HMB), and Vitamin D3. METHODS: Eighteen healthy strength-trained males were randomly assigned to a group that either consumed MT (n = 8, 22...
2016: Journal of the International Society of Sports Nutrition
https://www.readbyqxmd.com/read/27245589/a-peculiar-formula-of-essential-amino-acids-prevents-rosuvastatin-myopathy-in-mice
#18
Giuseppe D'Antona, Laura Tedesco, Chiara Ruocco, Giovanni Corsetti, Maurizio Ragni, Andrea Fossati, Elisa Saba, Francesca Fenaroli, Mery Montinaro, Michele Carruba, Alessandra Valerio, Enzo Nisoli
AIMS: Myopathy, characterized by mitochondrial oxidative stress, occurs in approximately 10 % of statin-treated patients, and a major risk exists with potent statins, such as rosuvastatin (Rvs). We sought to determine whether a selective branched-chain amino-acid-enriched mixture (BCAAem), found to improve mitochondrial function and reduce oxidative stress in muscle of middle-aged mice, was able to prevent Rvs myopathy. RESULTS: Dietary supplementation of BCAAem was able to prevent the structural and functional alterations of muscle induced by Rvs in young mice...
June 1, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27241020/loganin-possesses-neuroprotective-properties-restores-smn-protein-and-activates-protein-synthesis-positive-regulator-akt-mtor-in-experimental-models-of-spinal-muscular-atrophy
#19
Yu-Ting Tseng, Cheng-Sheng Chen, Yuh-Jyh Jong, Fang-Rong Chang, Yi-Ching Lo
Spinal muscular atrophy (SMA) is an autosomal recessive neurodegenerative disease characterized by motor neurons degeneration and muscular atrophy. There is no effective SMA treatment. Loganin is a botanical candidate with anti-inflammatory, anti-oxidant, glucose-lowering and anti-diabetic nephropathy activities. The aim of this study is to investigate the potential protective effects of loganin on SMA using two cellular models, SMN-deficient NSC34 cells and SMA patient fibroblasts, and an animal disease model, SMAΔ7 mice...
September 2016: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/27215286/the-emerging-role-of-viral-vectors-as-vehicles-for-dmd-gene-editing
#20
REVIEW
Ignazio Maggio, Xiaoyu Chen, Manuel A F V Gonçalves
Duchenne muscular dystrophy (DMD) is a genetic disorder caused by mutations in the dystrophin-encoding DMD gene. The DMD gene, spanning over 2.4 megabases along the short arm of the X chromosome (Xp21.2), is the largest genetic locus known in the human genome. The size of DMD, combined with the complexity of the DMD phenotype and the extent of the affected tissues, begs for the development of novel, ideally complementary, therapeutic approaches. Genome editing based on the delivery of sequence-specific programmable nucleases into dystrophin-defective cells has recently enriched the portfolio of potential therapies under investigation...
2016: Genome Medicine
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