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Skeletal Muscle

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https://www.readbyqxmd.com/read/29145886/are-mice-good-models-for-human-neuromuscular-disease-comparing-muscle-excursions-in-walking-between-mice-and-humans
#1
Xiao Hu, James P Charles, Turgay Akay, John R Hutchinson, Silvia S Blemker
BACKGROUND: The mouse is one of the most widely used animal models to study neuromuscular diseases and test new therapeutic strategies. However, findings from successful pre-clinical studies using mouse models frequently fail to translate to humans due to various factors. Differences in muscle function between the two species could be crucial but often have been overlooked. The purpose of this study was to evaluate and compare muscle excursions in walking between mice and humans. METHODS: Recently published musculoskeletal models of the mouse hindlimb and human lower limb were used to simulate muscle-tendon dynamics during mouse and human walking, a key daily activity...
November 16, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/29121992/a-mouse-anti-myostatin-antibody-increases-muscle-mass-and-improves-muscle-strength-and-contractility-in-the-mdx-mouse-model-of-duchenne-muscular-dystrophy-and-its-humanized-equivalent-domagrozumab-pf-06252616-increases-muscle-volume-in-cynomolgus-monkeys
#2
Michael St Andre, Mark Johnson, Prashant N Bansal, Jeremy Wellen, Andrew Robertson, Alan Opsahl, Peter M Burch, Peter Bialek, Carl Morris, Jane Owens
BACKGROUND: The treatments currently approved for Duchenne muscular dystrophy (DMD), a progressive skeletal muscle wasting disease, address the needs of only a small proportion of patients resulting in an urgent need for therapies that benefit all patients regardless of the underlying mutation. Myostatin is a member of the transforming growth factor-β (TGF-β) family of ligands and is a negative regulator of skeletal muscle mass. Loss of myostatin has been shown to increase muscle mass and improve muscle function in both normal and dystrophic mice...
November 9, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/29115986/the-breaking-and-making-of-healthy-adult-human-skeletal-muscle-in-vivo
#3
Abigail L Mackey, Michael Kjaer
BACKGROUND: While muscle regeneration has been extensively studied in animal and cell culture models, in vivo myogenesis in adult human skeletal muscle has not been investigated in detail. METHODS: Using forced lengthening contractions induced by electrical stimulation, we induced myofibre injury in young healthy males. Muscle biopsies were collected from the injured leg 7 and 30 days after muscle injury and from the uninjured leg as a control. Immuno-stained single muscle fibres and muscle cross sections were studied by wide-field and confocal microscopy...
November 7, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/29078808/treatment-with-the-anti-il-6-receptor-antibody-attenuates-muscular-dystrophy-via-promoting-skeletal-muscle-regeneration-in-dystrophin-utrophin-deficient-mice
#4
Eiji Wada, Jun Tanihata, Akira Iwamura, Shin'ichi Takeda, Yukiko K Hayashi, Ryoichi Matsuda
BACKGROUND: Chronic increases in the levels of the inflammatory cytokine interleukin-6 (IL-6) in serum and skeletal muscle are thought to contribute to the progression of muscular dystrophy. Dystrophin/utrophin double-knockout (dKO) mice develop a more severe and progressive muscular dystrophy than the mdx mice, the most common murine model of Duchenne muscular dystrophy (DMD). In particular, dKO mice have smaller body sizes and muscle diameters, and develop progressive kyphosis and fibrosis in skeletal and cardiac muscles...
October 27, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/29065908/utrophin-influences-mitochondrial-pathology-and-oxidative-stress-in-dystrophic-muscle
#5
Tahnee L Kennedy, Lee Moir, Sarah Hemming, Ben Edwards, Sarah Squire, Kay Davies, Simon Guiraud
BACKGROUND: Duchenne muscular dystrophy (DMD) is a lethal X-linked muscle wasting disorder caused by the absence of dystrophin, a large cytoskeletal muscle protein. Increasing the levels of the dystrophin-related-protein utrophin is a highly promising therapy for DMD and has been shown to improve pathology in dystrophin-deficient mice. One contributing factor to muscle wasting in DMD is mitochondrial pathology that contributes to oxidative stress and propagates muscle damage. The purpose of this study was to assess whether utrophin could attenuate mitochondria pathology and oxidative stress...
October 24, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/29047406/loss-of-mkp-5-promotes-myofiber-survival-by-activating-stat3-bcl-2-signaling-during-regenerative-myogenesis
#6
Kisuk Min, Ahmed Lawan, Anton M Bennett
BACKGROUND: The mitogen-activated protein kinases (MAPKs) have been shown to be involved in regulating myofiber survival. In skeletal muscle, p38 MAPK and JNK are negatively regulated by MAPK phosphatase-5 (MKP-5). During muscle regeneration, MKP-5 is downregulated, thereby promoting p38 MAPK/JNK signaling, and subsequent repair of damaged muscle. Mice lacking MKP-5 expression exhibit enhanced regenerative myogenesis. However, the effect of MKP-5 on myofiber survival during regeneration is unclear...
October 18, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/29017538/hgf-potentiates-extracellular-matrix-driven-migration-of-human-myoblasts-involvement-of-matrix-metalloproteinases-and-mapk-erk-pathway
#7
Mariela Natacha González, Wallace de Mello, Gillian S Butler-Browne, Suse Dayse Silva-Barbosa, Vincent Mouly, Wilson Savino, Ingo Riederer
BACKGROUND: The hepatocyte growth factor (HGF) is required for the activation of muscle progenitor cells called satellite cells (SC), plays a role in the migration of proliferating SC (myoblasts), and is present as a soluble factor during muscle regeneration, along with extracellular matrix (ECM) molecules. In this study, we aimed at determining whether HGF is able to interact with ECM proteins, particularly laminin 111 and fibronectin, and to modulate human myoblast migration. METHODS: We evaluated the expression of the HGF-receptor c-Met, laminin, and fibronectin receptors by immunoblotting, flow cytometry, or immunofluorescence and used Transwell assays to analyze myoblast migration on laminin 111 and fibronectin in the absence or presence of HGF...
October 10, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28899419/increased-plasma-lipid-levels-exacerbate-muscle-pathology-in-the-mdx-mouse-model-of-duchenne-muscular-dystrophy
#8
Nadia Milad, Zoe White, Arash Y Tehrani, Stephanie Sellers, Fabio M V Rossi, Pascal Bernatchez
BACKGROUND: Duchenne muscular dystrophy (DMD) is caused by loss of dystrophin expression and leads to severe ambulatory and cardiac function decline. However, the dystrophin-deficient mdx murine model of DMD only develops a very mild form of the disease. Our group and others have shown vascular abnormalities in animal models of MD, a likely consequence of the fact that blood vessels express the same dystrophin-associated glycoprotein complex (DGC) proteins as skeletal muscles. METHODS: To test the blood vessel contribution to muscle damage in DMD, mdx (4cv) mice were given elevated lipid levels via apolipoprotein E (ApoE) gene knockout combined with normal chow or lipid-rich Western diets...
September 12, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28882193/fragile-x-mental-retardation-protein-regulates-skeletal-muscle-stem-cell-activity-by-regulating-the-stability-of-myf5-mrna
#9
Ryo Fujita, Victoria Zismanov, Jean-Marie Jacob, Solène Jamet, Krum Asiev, Colin Crist
BACKGROUND: Regeneration of adult tissues relies on adult stem cells that are primed to enter a differentiation program, while typically remaining quiescent. In mouse skeletal muscle, these features are reconciled by multiple translational control mechanisms that ensure primed muscle stem cells (MuSCs) are not activated. In quiescent MuSCs, this concept is illustrated by reversible microRNA silencing of Myf5 translation, mediated by microRNA-31 and fragile X mental retardation protein (FMRP)...
September 7, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28870245/mice-overexpressing-growth-hormone-exhibit-increased-skeletal-muscle-myostatin-and-murf1-with-attenuation-of-muscle-mass
#10
Leslie A Consitt, Alicson Saneda, Gunjan Saxena, Edward O List, John J Kopchick
BACKGROUND: In contrast to the acute effects of growth hormone (GH) on skeletal muscle protein synthesis, long-term GH treatment appears to have negligible effects on muscle mass. Despite this knowledge, little is known regarding the chronic effects of GH on skeletal muscle protein synthesis and atrophy signaling pathways. The purpose of this study was to determine if protein synthesis pathways are attenuated and/or muscle atrophy intracellular signaling pathways are altered in the skeletal muscle of transgenic bovine GH (bGH) mice...
September 4, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28870238/bet-bromodomain-inhibitors-and-agonists-of-the-beta-2-adrenergic-receptor-identified-in-screens-for-compounds-that-inhibit-dux4-expression-in-fshd-muscle-cells
#11
Amy E Campbell, Jonathan Oliva, Matthew P Yates, Jun Wen Zhong, Sean C Shadle, Lauren Snider, Nikita Singh, Shannon Tai, Yosuke Hiramuki, Rabi Tawil, Silvère M van der Maarel, Stephen J Tapscott, Francis M Sverdrup
BACKGROUND: Facioscapulohumeral dystrophy (FSHD) is a progressive muscle disease caused by mutations that lead to epigenetic derepression and inappropriate transcription of the double homeobox 4 (DUX4) gene in skeletal muscle. Drugs that enhance the repression of DUX4 and prevent its expression in skeletal muscle cells therefore represent candidate therapies for FSHD. METHODS: We screened an aggregated chemical library enriched for compounds with epigenetic activities and the Pharmakon 1600 library composed of compounds that have reached clinical testing to identify molecules that decrease DUX4 expression as monitored by the levels of DUX4 target genes in FSHD patient-derived skeletal muscle cell cultures...
September 4, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28697784/exome-sequencing-reveals-independent-sgcd-deletions-causing-limb-girdle-muscular-dystrophy-in-boston-terriers
#12
Melissa L Cox, Jacquelyn M Evans, Alexander G Davis, Ling T Guo, Jennifer R Levy, Alison N Starr-Moss, Elina Salmela, Marjo K Hytönen, Hannes Lohi, Kevin P Campbell, Leigh Anne Clark, G Diane Shelton
BACKGROUND: Limb-girdle muscular dystrophies (LGMDs) are a heterogeneous group of inherited autosomal myopathies that preferentially affect voluntary muscles of the shoulders and hips. LGMD has been clinically described in several breeds of dogs, but the responsible mutations are unknown. The clinical presentation in dogs is characterized by marked muscle weakness and atrophy in the shoulder and hips during puppyhood. METHODS: Following clinical evaluation, the identification of the dystrophic histological phenotype on muscle histology, and demonstration of the absence of sarcoglycan-sarcospan complex by immunostaining, whole exome sequencing was performed on five Boston terriers: one affected dog and its three family members and one unrelated affected dog...
July 11, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28693603/differential-requirement-for-satellite-cells-during-overload-induced-muscle-hypertrophy-in-growing-versus-mature-mice
#13
Kevin A Murach, Sarah H White, Yuan Wen, Angel Ho, Esther E Dupont-Versteegden, John J McCarthy, Charlotte A Peterson
BACKGROUND: Pax7+ satellite cells are required for skeletal muscle fiber growth during post-natal development in mice. Satellite cell-mediated myonuclear accretion also appears to persist into early adulthood. Given the important role of satellite cells during muscle development, we hypothesized that the necessity of satellite cells for adaptation to an imposed hypertrophic stimulus depends on maturational age. METHODS: Pax7(CreER)-R26R(DTA) mice were treated for 5 days with vehicle (satellite cell-replete, SC+) or tamoxifen (satellite cell-depleted, SC-) at 2 months (young) and 4 months (mature) of age...
July 10, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28637492/expression-patterns-of-fshd-causing-dux4-and-myogenic-transcription-factors-pax3-and-pax7-are-spatially-distinct-in-differentiating-human-stem-cell-cultures
#14
Premi Haynes, Kelly Kernan, Suk-Lin Zhou, Daniel G Miller
BACKGROUND: Facioscapulohumeral muscular dystrophy (FSHD) is most commonly inherited in an autosomal dominant pattern and caused by the abnormal expression of DUX4 in skeletal muscle. The DUX4 transcription factor has DNA binding domains similar to several paired class homeotic transcription factors, but only myogenic factors PAX3 and PAX7 rescue cell viability when co-expressed with DUX4 in mouse myoblasts. This observation suggests competition for DNA binding sites in satellite cells might limit muscle repair and may be one aspect of DUX4-associated myotoxicity...
June 21, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28587678/smchd1-regulates-a-limited-set-of-gene-clusters-on-autosomal-chromosomes
#15
Amanda G Mason, Roderick C Slieker, Judit Balog, Richard J L F Lemmers, Chao-Jen Wong, Zizhen Yao, Jong-Won Lim, Galina N Filippova, Enrico Ne, Rabi Tawil, Bas T Heijmans, Stephen J Tapscott, Silvère M van der Maarel
BACKGROUND: Facioscapulohumeral muscular dystrophy (FSHD) is in most cases caused by a contraction of the D4Z4 macrosatellite repeat on chromosome 4 (FSHD1) or by mutations in the SMCHD1 or DNMT3B gene (FSHD2). Both situations result in the incomplete epigenetic repression of the D4Z4-encoded retrogene DUX4 in somatic cells, leading to the aberrant expression of DUX4 in the skeletal muscle. In mice, Smchd1 regulates chromatin repression at different loci, having a role in CpG methylation establishment and/or maintenance...
June 6, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28587652/nanospan-an-alternatively-spliced-isoform-of-sarcospan-localizes-to-the-sarcoplasmic-reticulum-in-skeletal-muscle-and-is-absent-in-limb-girdle-muscular-dystrophy-2f
#16
Angela K Peter, Gaynor Miller, Joana Capote, Marino DiFranco, Alhondra Solares-Pérez, Emily L Wang, Jim Heighway, Ramón M Coral-Vázquez, Julio Vergara, Rachelle H Crosbie-Watson
BACKGROUND: Sarcospan (SSPN) is a transmembrane protein that interacts with the sarcoglycans (SGs) to form a tight subcomplex within the dystrophin-glycoprotein complex that spans the sarcolemma and interacts with laminin in the extracellular matrix. Overexpression of SSPN ameliorates Duchenne muscular dystrophy in murine models. METHODS: Standard cloning approaches were used to identify nanospan, and nanospan-specific polyclonal antibodies were generated and validated...
June 6, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28571586/complement-c5a-c5ar1-signalling-drives-skeletal-muscle-macrophage-recruitment-in-the-hsod1-g93a-mouse-model-of-amyotrophic-lateral-sclerosis
#17
Haitao A Wang, John D Lee, Kah Meng Lee, Trent M Woodruff, Peter G Noakes
BACKGROUND: The terminal pathway of the innate immune complement system is implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Terminal complement activation leads to generation of C5a, which through its receptor, C5aR1, drives immune cell recruitment and activation. Importantly, genetic or pharmacological blockage of C5aR1 improves motor performance and reduces disease pathology in hSOD1(G93A) rodent models of ALS. In this study, we aimed to explore the potential mechanisms of C5aR1-mediated pathology in hSOD1(G93A) mice by examining their skeletal muscles...
June 1, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28526070/the-golden-retriever-model-of-duchenne-muscular-dystrophy
#18
REVIEW
Joe N Kornegay
Duchenne muscular dystrophy (DMD) is an X-linked disease caused by mutations in the DMD gene and loss of the protein dystrophin. The absence of dystrophin leads to myofiber membrane fragility and necrosis, with eventual muscle atrophy and contractures. Affected boys typically die in their second or third decade due to either respiratory failure or cardiomyopathy. Despite extensive attempts to develop definitive therapies for DMD, the standard of care remains prednisone, which has only palliative benefits. Animal models, mainly the mdx mouse and golden retriever muscular dystrophy (GRMD) dog, have played a key role in studies of DMD pathogenesis and treatment development...
May 19, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28506310/unexpected-evolutionarily-conserved-rapid-effects-of-viral-infection-on-oxytocin-receptor-and-tgf-%C3%AE-psmad3
#19
Yutong Liu, Irina Conboy
BACKGROUND: shRNA lentiviral vectors are extensively used for gene knockdowns in mammalian cells, and non-target shRNAs typically are considered the proper experimental control for general changes caused by RNAi. However, the effects of non-target lentivirus controls on the modulation of cell signaling pathways remain largely unknown. In this study, we evaluated the effect of control lentiviral transduction on oxytocin receptor (OXTR) expression through the ERK/MAPK pathway in mouse and human skeletal muscle cells, on myogenic activity, and in vivo on mouse muscle regeneration...
May 15, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28526071/retinoid-acid-induced-microrna-31-5p-suppresses-myogenic-proliferation-and-differentiation-by-targeting-camkii%C3%AE
#20
Bo Liu, Chao Liu, Wei Cong, Nan Li, Nan Zhou, Yi Tang, Chao Wei, Han Bai, Ying Zhang, Jing Xiao
BACKGROUND: We previously reported that Wnt5a/CaMKIIδ (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Our latest study found that the expression of miR-31-5p, which was predicted to target the 3'UTR of CamkIIδ, was raised in the RA-treated embryonic tongue. Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKIIδ pathway through miR-31-5p in embryonic tongue. METHODS: C2C12 myoblast line was employed as an in vitro model to examine the suppression of miR-31-5p on CamkIIδ expression, through which RA impaired the myoblast proliferation and differentiation in embryonic tongue...
May 11, 2017: Skeletal Muscle
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