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https://www.readbyqxmd.com/read/27920252/group-i-paks-promote-skeletal-myoblast-differentiation-in-vivo-and-in-vitro
#1
Giselle A Joseph, Min Lu, Maria Radu, Jennifer K Lee, Steven J Burden, Jonathan Chernoff, Robert S Krauss
Skeletal myogenesis is regulated by signal transduction, but the factors and mechanisms involved are not well understood. The group I Paks, Pak1 and Pak2, are related protein kinases and direct effectors of Cdc42 and Rac1. Group I Paks are ubiquitously expressed and specifically required for myoblast fusion in Drosophila We report that both Pak1 and Pak2 are activated during mammalian myoblast differentiation. One pathway of activation is initiated by N-cadherin ligation, and involves the cadherin co-receptor Cdo with its downstream effector, Cdc42...
December 5, 2016: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/27906114/p38%C3%AE-mapk-disables-kmt1a-mediated-repression-of-myogenic-differentiation-program
#2
Biswanath Chatterjee, David W Wolff, Mathivanan Jothi, Munmun Mal, Asoke K Mal
BACKGROUND: Master transcription factor MyoD can initiate the entire myogenic gene expression program which differentiates proliferating myoblasts into multinucleated myotubes. We previously demonstrated that histone methyltransferase KMT1A associates with and inhibits MyoD in proliferating myoblasts, and must be removed to allow differentiation to proceed. It is known that pro-myogenic signaling pathways such as PI3K/AKT and p38α MAPK play critical roles in enforcing associations between MyoD and transcriptional activators, while removing repressors...
August 22, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906101/characterization-of-a-dmd-egfp-reporter-mouse-as-a-tool-to-investigate-dystrophin-expression
#3
Mina V Petkova, Susanne Morales-Gonzales, Karima Relizani, Esther Gill, Franziska Seifert, Josefine Radke, Werner Stenzel, Luis Garcia, Helge Amthor, Markus Schuelke
BACKGROUND: Dystrophin is a rod-shaped cytoplasmic protein that provides sarcolemmal stability as a structural link between the cytoskeleton and the extracellular matrix via the dystrophin-associated protein complex (DAPC). Mutations in the dystrophin-encoding DMD gene cause X-linked dystrophinopathies with variable phenotypes, the most severe being Duchenne muscular dystrophy (DMD) characterized by progressive muscle wasting and fibrosis. However, dystrophin deficiency does not only impair the function of skeletal and heart muscle but may also affect other organ systems such as the brain, eye, and gastrointestinal tract...
July 5, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906098/direct-reprogramming-of-urine-derived-cells-with-inducible-myod-for-modeling-human-muscle-disease
#4
Ellis Y Kim, Patrick Page, Lisa M Dellefave-Castillo, Elizabeth M McNally, Eugene J Wyatt
BACKGROUND: Cellular models of muscle disease are taking on increasing importance with the large number of genes and mutations implicated in causing myopathies and the concomitant need to test personalized therapies. Developing cell models relies on having an easily obtained source of cells, and if the cells are not derived from muscle itself, a robust reprogramming process is needed. Fibroblasts are a human cell source that works well for the generation of induced pluripotent stem cells, which can then be differentiated into cardiomyocyte lineages, and with less efficiency, skeletal muscle-like lineages...
September 15, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906075/nuclear-bodies-reorganize-during-myogenesis-in-vitro-and-are-differentially-disrupted-by-expression-of-fshd-associated-dux4
#5
Sachiko Homma, Mary Lou Beermann, Bryant Yu, Frederick M Boyce, Jeffrey Boone Miller
BACKGROUND: Nuclear bodies, such as nucleoli, PML bodies, and SC35 speckles, are dynamic sub-nuclear structures that regulate multiple genetic and epigenetic processes. Additional regulation is provided by RNA/DNA handling proteins, notably TDP-43 and FUS, which have been linked to ALS pathology. Previous work showed that mouse cell line myotubes have fewer but larger nucleoli than myoblasts, and we had found that nuclear aggregation of TDP-43 in human myotubes was induced by expression of DUX4-FL, a transcription factor that is aberrantly expressed and causes pathology in facioscapulohumeral dystrophy (FSHD)...
December 1, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906069/the-beneficial-role-of-proteolysis-in-skeletal-muscle-growth-and-stress-adaptation
#6
REVIEW
Ryan A V Bell, Mohammad Al-Khalaf, Lynn A Megeney
Muscle atrophy derived from excessive proteolysis is a hallmark of numerous disease conditions. Accordingly, the negative consequences of skeletal muscle protein breakdown often overshadow the critical nature of proteolytic systems in maintaining normal cellular function. Here, we discuss the major cellular proteolysis machinery-the ubiquitin/proteosome system, the autophagy/lysosomal system, and caspase-mediated protein cleavage-and the critical role of these protein machines in establishing and preserving muscle health...
April 6, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906063/characterization-of-a-multiprotein-complex-involved-in-excitation-transcription-coupling-of-skeletal-muscle
#7
Manuel Arias-Calderón, Gonzalo Almarza, Alexis Díaz-Vegas, Ariel Contreras-Ferrat, Denisse Valladares, Mariana Casas, Héctor Toledo, Enrique Jaimovich, Sonja Buvinic
BACKGROUND: Electrical activity regulates the expression of skeletal muscle genes by a process known as "excitation-transcription" (E-T) coupling. We have demonstrated that release of adenosine 5'-triphosphate (ATP) during depolarization activates membrane P2X/P2Y receptors, being the fundamental mediators between electrical stimulation, slow intracellular calcium transients, and gene expression. We propose that this signaling pathway would require the proper coordination between the voltage sensor (dihydropyridine receptor, DHPR), pannexin 1 channels (Panx1, ATP release conduit), nucleotide receptors, and other signaling molecules...
April 11, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906051/the-lysine-methyltransferase-ehmt2-g9a-is-dispensable-for-skeletal-muscle-development-and-regeneration
#8
Regan-Heng Zhang, Robert N Judson, David Y Liu, Jürgen Kast, Fabio M V Rossi
BACKGROUND: Euchromatic histone-lysine N-methyltransferase 2 (G9a/Ehmt2) is the main enzyme responsible for the apposition of H3K9 di-methylation on histones. Due to its dual role as an epigenetic regulator and in the regulation of non-histone proteins through direct methylation, G9a has been implicated in a number of biological processes relevant to cell fate control. Recent reports employing in vitro cell lines indicate that Ehmt2 methylates MyoD to repress its transcriptional activity and therefore its ability to induce differentiation of activated myogenic cells...
May 27, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27905294/glucocorticoids-increase-skeletal-muscle-nf-%C3%AE%C2%BAb-inducing-kinase-nik-links-to-muscle-atrophy
#9
Christopher S Fry, Syed Z Nayeem, Edgar L Dillon, Partha S Sarkar, Batbayar Tumurbaatar, Randall J Urban, Traver J Wright, Melinda Sheffield-Moore, Ronald G Tilton, Sanjeev Choudhary
Glucocorticoids (GC) are a frontline therapy for numerous acute and chronic diseases because of their demonstrated efficacy at reducing systemic inflammation. An unintended side effect of GC therapy is the stimulation of skeletal muscle atrophy. Pathophysiological mechanisms responsible for GC-induced skeletal muscle atrophy have been extensively investigated, and the ability to treat patients with GC without unintended muscle atrophy has yet to be realized. We have reported that a single, standard-of-care dose of Methylprednisolone increases in vivo expression of NF-κB-inducing kinase (NIK), an important upstream regulatory kinase controlling NF-κB activation, along with other key muscle catabolic regulators such as Atrogin-1 and MuRF1 that induce skeletal muscle proteolysis...
November 2016: Physiological Reports
https://www.readbyqxmd.com/read/27897418/suppression-of-muscle-wasting-by-the-plant-derived-compound-ursolic-acid-in-a-model-of-chronic-kidney-disease
#10
Rizhen Yu, Ji-An Chen, Jing Xu, Jin Cao, Yanlin Wang, Sandhya S Thomas, Zhaoyong Hu
BACKGROUND: Muscle wasting in chronic kidney disease (CKD) and other catabolic disorders contributes to morbidity and mortality, and there are no therapeutic interventions that regularly and safely block losses of muscle mass. We have obtained evidence that impaired IGF-1/insulin signalling and increases in glucocorticoids, myostatin and/or inflammatory cytokines that contribute to the development of muscle wasting in catabolic disorders by activating protein degradation. METHODS: Using in vitro and in vivo models of muscle wasting associated with CKD or dexamethasone administration, we measured protein synthesis and degradation and examined mechanisms by which ursolic acid, derived from plants, could block the loss of muscle mass stimulated by CKD or excessive levels of dexamethasone...
November 17, 2016: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/27897407/activin-a-induces-skeletal-muscle-catabolism-via-p38%C3%AE-mitogen-activated-protein-kinase
#11
Hui Ding, Guohua Zhang, Ka Wai Thomas Sin, Zhelong Liu, Ren-Kuo Lin, Min Li, Yi-Ping Li
BACKGROUND: Activation of type IIB activin receptor (ActRIIB) in skeletal muscle leads to muscle atrophy because of increased muscle protein degradation. However, the intracellular signalling mechanism that mediates ActRIIB-activated muscle catabolism is poorly defined. METHODS: We investigated the role of p38β mitogen-activated protein kinases (MAPK) in mediating ActRIIB ligand activin A-activated muscle catabolic pathways in C2C12 myotubes and in mice with perturbation of this kinase pharmacologically and genetically...
September 16, 2016: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/27895387/retention-of-acetylcarnitine-in-chronic-kidney-disease-causes-insulin-resistance-in-skeletal-muscle
#12
Yasunori Miyamoto, Teruo Miyazaki, Akira Honda, Homare Shimohata, Kouichi Hirayama, Masaki Kobayashi
Insulin resistance occurs frequently in patients with chronic kidney disease. However, the mechanisms of insulin resistance associated with chronic kidney disease are unclear. It is known that an increase in the mitochondrial acetyl-CoA (AcCoA)/CoA ratio causes insulin resistance in skeletal muscle, and this ratio is regulated by carnitine acetyltransferase that exchanges acetyl moiety between CoA and carnitine. Because excess acetyl moiety of AcCoA is excreted in urine as acetylcarnitine, we hypothesized that retention of acetylcarnitine might be a cause of insulin resistance in chronic kidney disease patients...
November 2016: Journal of Clinical Biochemistry and Nutrition
https://www.readbyqxmd.com/read/27882542/a-novel-gain-of-function-mutation-in-orai1-causes-late-onset-tubular-aggregate-myopathy-and-congenital-miosis
#13
M Garibaldi, F Fattori, B Riva, C Labasse, G Brochier, P Ottaviani, S Sacconi, E Vizzaccaro, F Laschena, N B Romero, A Genazzani, E Bertini, G Antonini
We present three members of an Italian family affected by tubular aggregate myopathy (TAM) and congenital miosis harboring a novel missense mutation in ORAI1. All patients had a mild, late onset TAM revealed by asymptomatic creatine kinase (CK) elevation and congenital miosis consistent with a Stormorken-like Syndrome, in the absence of thrombocytopathy. Muscle biopsies showed classical histological findings but ultrastructural analysis revealed atypical tubular aggregates (TAs). The whole body muscle magnetic resonance imaging (MRI) showed a similar pattern of muscle involvement that correlated with clinical severity...
October 13, 2016: Clinical Genetics
https://www.readbyqxmd.com/read/27879669/synthesis-of-a-morpholino-nucleic-acid-mna-uridine-phosphoramidite-and-exon-skipping-using-mna-2-o-methyl-mixmer-antisense-oligonucleotide
#14
Suxiang Chen, Bao T Le, Kamal Rahimizadeh, Khalil Shaikh, Narinder Mohal, Rakesh N Veedu
In this study, we synthesised a morpholino nucleoside-uridine (MNA-U) phosphoramidite and evaluated the potential of a MNA-modified antisense oligonucleotide (AO) sequences to induce exon 23 skipping in mdx mouse myotubes in vitro towards extending the applicability of morpholino chemistry with other nucleotide monomers. We designed, synthesised, and compared exon skipping efficiencies of 20 mer MNA-modified 2'-O-methyl RNA mixmer AO on a phosphorothioate backbone (MNA/2'-OMePS) to the corresponding fully modified 2'-O-methyl RNA AO (2'-OMePS) as a control...
November 22, 2016: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/27878977/silk-fibroin-scaffolds-with-muscle-like-elasticity-support-in-vitro-differentiation-of-human-skeletal-muscle-cells
#15
Vishal Chaturvedi, Deboki Naskar, Beverley F Kinnear, Elizabeth Grenik, Danielle E Dye, Miranda D Grounds, Subhas C Kundu, Deirdre R Coombe
Human adult skeletal muscle has a limited ability to regenerate after injury and therapeutic options for volumetric muscle loss are few. Technologies to enhance regeneration of tissues generally rely upon bioscaffolds to mimic aspects of the tissue extracellular matrix (ECM). In the present study, silk fibroins from four Lepidoptera (silkworm) species engineered into three-dimensional scaffolds were examined for their ability to support the differentiation of primary human skeletal muscle myoblasts. Human skeletal muscle myoblasts (HSMMs) adhered, spread and deposited extensive ECM on all the scaffolds, but immunofluorescence and quantitative polymerase chain reaction analysis of gene expression revealed that myotube formation occurred differently on the various scaffolds...
November 22, 2016: Journal of Tissue Engineering and Regenerative Medicine
https://www.readbyqxmd.com/read/27865007/anisotropic-materials-for-skeletal-muscle-tissue-engineering
#16
Soumen Jana, Sheeny K Lan Levengood, Miqin Zhang
Repair of damaged skeletal-muscle tissue is limited by the regenerative capacity of the native tissue. Current clinical approaches are not optimal for the treatment of large volumetric skeletal-muscle loss. As an alternative, tissue engineering represents a promising approach for the functional restoration of damaged muscle tissue. A typical tissue-engineering process involves the design and fabrication of a scaffold that closely mimics the native skeletal-muscle extracellular matrix (ECM), allowing organization of cells into a physiologically relevant 3D architecture...
November 16, 2016: Advanced Materials
https://www.readbyqxmd.com/read/27864687/omega-3-fatty-acid-epa-improves-regenerative-capacity-of-mouse-skeletal-muscle-cells-exposed-to-saturated-fat-and-inflammation
#17
Amarjit Saini, Adam P Sharples, Nasser Al-Shanti, Claire E Stewart
Sarcopenic obesity is characterised by high fat mass, low muscle mass and an elevated inflammatory environmental milieu. We therefore investigated the effects of elevated inflammatory cytokine TNF-α (aging/obesity) and saturated fatty acid, palmitate (obesity) on skeletal muscle cells in the presence/absence of EPA, a-3 polyunsaturated fatty acid with proposed anti-inflammatory, anti-obesity activities. In the present study we show that palmitate was lipotoxic, inducing high levels of cell death and blocking myotube formation...
November 18, 2016: Biogerontology
https://www.readbyqxmd.com/read/27856964/neonatal-satellite-cells-form-small-myotubes-in-vitro
#18
P L Carvajal Monroy, S Grefte, A M Kuijpers-Jagtman, J W Von den Hoff, F A D T G Wagener
Although palatal muscle reconstruction in patients with cleft palate takes place during early childhood, normal speech development is often not achieved. We hypothesized that the intrinsic properties of head satellite cells (SCs) and the young age of these patients contribute to the poor muscle regeneration after surgery. First, we studied the fiber type distribution and the expression of SC markers in ex vivo muscle tissue from head (branchiomeric) and limb (somite-derived) muscles from neonatal (2-wk-old) and young (9-wk-old) rats...
November 16, 2016: Journal of Dental Research
https://www.readbyqxmd.com/read/27834030/does-the-grass-snake-natrix-natrix-squamata-serpentes-natricinae-fit-the-amniotes-specific-model-of-myogenesis
#19
Damian Lewandowski, Magda Dubińska-Magiera, Ewelina Posyniak, Weronika Rupik, Małgorzata Daczewska
In the grass snake (Natrix natrix), the newly developed somites form vesicles that are located on both sides of the neural tube. The walls of the vesicles are composed of tightly connected epithelial cells surrounding the cavity (the somitocoel). Also, in the newly formed somites, the Pax3 protein can be observed in the somite wall cells. Subsequently, the somite splits into three compartments: the sclerotome, dermomyotome (with the dorsomedial [DM] and the ventrolateral [VL] lips) and the myotome. At this stage, the Pax3 protein is detected in both the DM and VL lips of the dermomyotome and in the mononucleated cells of the myotome, whereas the Pax7 protein is observed in the medial part of the dermomyotome and in some of the mononucleated cells of the myotome...
November 10, 2016: Protoplasma
https://www.readbyqxmd.com/read/27833566/evidence-for-altered-ca-2-handling-in-growth-associated-protein-43-knockout-skeletal-muscle
#20
Giusy A Caprara, Caterina Morabito, Stefano Perni, Riccardo Navarra, Simone Guarnieri, Maria A Mariggiò
Neuronal growth-associated protein 43 (GAP43) has crucial roles in the nervous system, and during development, regeneration after injury, and learning and memory. GAP43 is expressed in mouse skeletal muscle fibers and satellite cells, with suggested its involvement in intracellular Ca(2+) handling. However, the physiological role of GAP43 in muscle remains unknown. Using a GAP43-knockout (GAP43(-/-)) mouse, we have defined the role of GAP43 in skeletal muscle. GAP43(-/-) mice showed low survival beyond weaning, reduced adult body weight, decreased muscle strength, and changed myofiber ultrastructure, with no significant differences in the expression of markers of satellite cell and myotube progression through the myogenic program...
2016: Frontiers in Physiology
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