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Muscular Regeneration

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https://www.readbyqxmd.com/read/27908613/sparc-interacts-with-actin-in-skeletal-muscle-in%C3%A2-vitro-and-in%C3%A2-vivo
#1
Louise H Jørgensen, Pia Lørup Jepsen, Anders Boysen, Line B Dalgaard, Lars G Hvid, Niels Ørtenblad, Dea Ravn, Jeeva Sellathurai, Jakob Møller-Jensen, Hanns Lochmüller, Henrik D Schrøder
The cytoskeleton is an integral part of skeletal muscle structure, and reorganization of the cytoskeleton occurs during various modes of remodeling. We previously found that the extracellular matrix protein secreted protein acidic and rich in cysteine (SPARC) is up-regulated and expressed intracellularly in developing muscle, during regeneration and in myopathies, which together suggests that SPARC might serve a specific role within muscle cells. Using co-immunoprecipitation combined with mass spectrometry and verified by staining for direct protein-protein interaction, we find that SPARC binds to actin...
November 28, 2016: American Journal of Pathology
https://www.readbyqxmd.com/read/27906106/loss-of-niche-satellite-cell-interactions-in-syndecan-3-null-mice-alters-muscle-progenitor-cell-homeostasis-improving-muscle-regeneration
#2
Addolorata Pisconti, Glen B Banks, Farshad Babaeijandaghi, Nicole Dalla Betta, Fabio M V Rossi, Jeffrey S Chamberlain, Bradley B Olwin
BACKGROUND: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells. RESULTS: Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts...
October 4, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906065/dystrophin-deficient-dogs-with-reduced-myostatin-have-unequal-muscle-growth-and-greater-joint-contractures
#3
Joe N Kornegay, Daniel J Bogan, Janet R Bogan, Jennifer L Dow, Jiahui Wang, Zheng Fan, Naili Liu, Leigh C Warsing, Robert W Grange, Mihye Ahn, Cynthia J Balog-Alvarez, Steven W Cotten, Monte S Willis, Candice Brinkmeyer-Langford, Hongtu Zhu, Joe Palandra, Carl A Morris, Martin A Styner, Kathryn R Wagner
BACKGROUND: Myostatin (Mstn) is a negative regulator of muscle growth whose inhibition promotes muscle growth and regeneration. Dystrophin-deficient mdx mice in which myostatin is knocked out or inhibited postnatally have a less severe phenotype with greater total mass and strength and less fibrosis and fatty replacement of muscles than mdx mice with wild-type myostatin expression. Dogs with golden retriever muscular dystrophy (GRMD) have previously been noted to have increased muscle mass and reduced fibrosis after systemic postnatal myostatin inhibition...
April 4, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906064/treatment-with-rgdf11-does-not-improve-the-dystrophic-muscle-pathology-of-mdx-mice
#4
Fabrizio Rinaldi, Yu Zhang, Ricardo Mondragon-Gonzalez, Jeffrey Harvey, Rita C R Perlingeiro
BACKGROUND: Duchenne muscular dystrophy (DMD) is an inherited lethal muscle wasting disease characterized by cycles of degeneration and regeneration, with no effective therapy. Growth differentiation factor 11 (GDF11), a member of the TGF-β superfamily and myostatin homologous, has been reported to have the capacity to reverse age-related skeletal muscle loss. These initial findings led us to investigate the ability of GDF11 to promote regeneration in the context of muscular dystrophy and determine whether it could be a candidate to slow down or reverse the disease progression in DMD...
June 14, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27904496/adipose-derived-stem-cells-enhance-myogenic-differentiation-in-the-mdx-mouse-model-of-muscular-dystrophy-via-paracrine-signaling
#5
Ji-Qing Cao, Ying-Yin Liang, Ya-Qin Li, Hui-Li Zhang, Yu-Ling Zhu, Jia Geng, Li-Qing Yang, Shan-Wei Feng, Juan Yang, Jie Kong, Cheng Zhang
Adipose-derived stem cells have been shown to promote peripheral nerve regeneration through the paracrine secretion of neurotrophic factors. However, it is unclear whether these cells can promote myogenic differentiation in muscular dystrophy. Adipose-derived stem cells (6 × 10(6)) were injected into the gastrocnemius muscle of mdx mice at various sites. Dystrophin expression was found in the muscle fibers. Phosphorylation levels of Akt, mammalian target of rapamycin (mTOR), eIF-4E binding protein 1 and S6 kinase 1 were increased, and the Akt/mTOR pathway was activated...
October 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27897416/curcumin-an-effective-adjunct-in-patients-with-statin-associated-muscle-symptoms
#6
REVIEW
Amirhossein Sahebkar, Nikou Saboni, Matteo Pirro, Maciej Banach
In spite of the unequivocal efficacy of statins in reducing primary and secondary cardiovascular events, the use of these drugs in a considerable number of patients is limited because of statin intolerance, mainly statin-associated muscle symptoms (SAMS). SAMS encompass a broad spectrum of clinical presentations, including mild muscular aching and other types of myalgias, myopathy with the significant elevation of creatine kinase, and the rare but life-threatening rhabdomyolysis. Among several pathophysiologic mechanisms of SAMS, mitochondrial dysfunction is thought to be one of the main one...
September 22, 2016: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/27891608/compensatory-axon-sprouting-for-very-slow-axonal-die-back-in-a-transgenic-model-of-spinal-muscular-atrophy-type-iii
#7
Esther Udina, Charles Putman, Luke Harris, N Tyreman, Victoria Cook, Tessa Gordon
Spinal muscular atrophy (SMA) is a common autosomal recessive disorder in humans and is the leading genetic cause of infantile death. Patients lack the SMN1 gene with the severity of the disease depending on the number of copies of the highly homologous SMN2 gene. Although motoneuron death in the Smn+/- transgenic mouse model of mildest form of SMA, SMA type III, has been reported, we have used retrograde tracing of sciatic and femoral motoneurons in the hindlimb with recording of muscle and motor unit isometric forces to count the number of motoneurons with intact neuromuscular connections...
November 28, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27876000/comparison-of-repair-of-peripheral-nerve-transection-in-predegenerated-muscle-with-and-without-a-vein-graft
#8
Jamshid Mohammadi, Hamdollah Delaviz, Bahram Mohammadi, Hamoun Delaviz, Parastou Rad
BACKGROUND: Despite substantial research into the topic and valiant surgical efforts, reconstruction of peripheral nerve injury remains a challenging surgery. This study was conducted to evaluate the effectiveness of axonal regeneration of a transected sciatic nerve through a vein conduit containing degenerated skeletal muscle compared with axonal regeneration in a transected sciatic nerve through degenerated skeletal muscle alone. METHODS: In two of the three experimental rat groups, 10 mm of the left sciatic nerve was transected and removed...
November 22, 2016: BMC Neurology
https://www.readbyqxmd.com/read/27859236/postnatal-hyperplasic-effects-of-actriib-blockade-in-a-severely-dystrophic-muscle
#9
C Nielsen, R M Potter, C Borowy, K Jacinto, R Kumar, C G Carlson
The efficacy of two ActRIIB ligand trapping agents (RAP-031, RAP-435) in treating muscular dystrophy was examined by determining their morphological effects on the severely dystrophic triangularis sterni (TS) muscle of the mdx mouse, a model for Duchenne muscular dystrophy. These agents trap all endogenous ligands to the ActRIIB receptor and thereby block myostatin signaling in a highly selective manner. Short (1 month) and long term (3 months) in vivo treatment of 1 month old mdx mice increased myonuclei and fiber cross section (FCS) density but did not alter individual fiber size...
November 18, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27807076/a-poglut1-mutation-causes-a-muscular-dystrophy-with-reduced-notch-signaling-and-satellite-cell-loss
#10
Emilia Servián-Morilla, Hideyuki Takeuchi, Tom V Lee, Jordi Clarimon, Fabiola Mavillard, Estela Area-Gómez, Eloy Rivas, Jose L Nieto-González, Maria C Rivero, Macarena Cabrera-Serrano, Leonardo Gómez-Sánchez, Jose A Martínez-López, Beatriz Estrada, Celedonio Márquez, Yolanda Morgado, Xavier Suárez-Calvet, Guillermo Pita, Anne Bigot, Eduard Gallardo, Rafael Fernández-Chacón, Michio Hirano, Robert S Haltiwanger, Hamed Jafar-Nejad, Carmen Paradas
Skeletal muscle regeneration by muscle satellite cells is a physiological mechanism activated upon muscle damage and regulated by Notch signaling. In a family with autosomal recessive limb-girdle muscular dystrophy, we identified a missense mutation in POGLUT1 (protein O-glucosyltransferase 1), an enzyme involved in Notch posttranslational modification and function. In vitro and in vivo experiments demonstrated that the mutation reduces O-glucosyltransferase activity on Notch and impairs muscle development...
November 2, 2016: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/27783047/camkk2-suppresses-muscle-regeneration-through-the-inhibition-of-myoblast-proliferation-and-differentiation
#11
Cheng Ye, Duo Zhang, Lei Zhao, Yan Li, Xiaohan Yao, Hui Wang, Shengjie Zhang, Wei Liu, Hongchao Cao, Shuxian Yu, Yucheng Wang, Jingjing Jiang, Hui Wang, Xihua Li, Hao Ying
Skeletal muscle has a major role in locomotion and muscle disorders are associated with poor regenerative efficiency. Therefore, a deeper understanding of muscle regeneration is needed to provide a new insight for new therapies. CaMKK2 plays a role in the calcium/calmodulin-dependent kinase cascade; however, its role in skeletal muscle remains unknown. Here, we found that CaMKK2 expression levels were altered under physiological and pathological conditions including postnatal myogensis, freeze or cardiotoxin-induced muscle regeneration, and Duchenne muscular dystrophy...
October 24, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27777947/expansion-of-submucosal-bladder-wall-tissue-in-vitro-and-in-vivo
#12
Gisela Reinfeldt Engberg, Clara Ibel Chamorro, Agneta Nordenskjöld, Magdalena Fossum
In order to develop autologous tissue engineering of the whole wall in the urinary excretory system, we studied the regenerative capacity of the muscular bladder wall. Smooth muscle cell expansion on minced detrusor muscle in vitro and in vivo with or without urothelial tissue was studied. Porcine minced detrusor muscle and urothelium were cultured in vitro under standard culture conditions for evaluation of the explant technique and in collagen for tissue sectioning and histology. Autografts of minced detrusor muscle with or without minced urothelium were expanded on 3D cylinder moulds by grafting into the subcutaneous fat of the pig abdominal wall...
2016: BioMed Research International
https://www.readbyqxmd.com/read/27762666/different-donors-mesenchymal-stromal-cells-secretomes-reveal-heterogeneous-profile-of-relevance-for-therapeutic-use
#13
Amanda Faria Assoni, Giuliana Castello, Marcos Valadares, Melinda Beccari, Juliana Gomes, Mayra Pelatti, Miguel Mitne-Neto, Valdemir Melechco Carvalho, Mayana Zatz
Duchenne muscular dystrophy (DMD) is a lethal X-linked disorder caused by null mutations in the dystrophin gene. Although the primary defect is the deficiency of muscle dystrophin, secondary events, including chronic inflammation, fibrosis and muscle regeneration failure are thought to actively contribute to disease progression. Despite several advances, there is still no effective therapy for DMD. Therefore, the potential regenerative capacities, as well as immune-privileged properties of Mesenchymal Stromal Cells (MSCs), have been the focus of intense investigation in different animal models aiming the treatment of these disorders...
October 20, 2016: Stem Cells and Development
https://www.readbyqxmd.com/read/27760216/nitric-oxide-donor-molsidomine-positively-modulates-myogenic-differentiation-of-embryonic-endothelial-progenitors
#14
Mario Tirone, Valentina Conti, Fabio Manenti, Pier Andrea Nicolosi, Cristina D'Orlando, Emanuele Azzoni, Silvia Brunelli
Embryonic VE-Cadherin-expressing progenitors (eVE-Cad+), including hemogenic endothelium, have been shown to generate hematopoietic stem cells and a variety of other progenitors, including mesoangioblasts, or MABs. MABs are vessel-associated progenitors with multilineage mesodermal differentiation potential that can physiologically contribute to skeletal muscle development and regeneration, and have been used in an ex vivo cell therapy setting for the treatment of muscular dystrophy. There is currently a therapeutic need for molecules that could improve the efficacy of cell therapy protocols; one such good candidate is nitric oxide...
2016: PloS One
https://www.readbyqxmd.com/read/27758734/-cell-autonomous-defects-in-satellite-cells-impair-muscle-regeneration-in-duchenne-muscular-dystrophy
#15
Caroline E Brun, Nicolas A Dumont
No abstract text is available yet for this article.
October 2016: Médecine Sciences: M/S
https://www.readbyqxmd.com/read/27757223/loss-of-niche-satellite-cell-interactions-in-syndecan-3-null-mice-alters-muscle-progenitor-cell-homeostasis-improving-muscle-regeneration
#16
Addolorata Pisconti, Glen B Banks, Farshad Babaeijandaghi, Nicole Dalla Betta, Fabio M V Rossi, Jeffrey S Chamberlain, Bradley B Olwin
BACKGROUND: The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells. RESULTS: Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts...
2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27752168/-magnetic-resonance-imaging-of-dystrophinopathy-that-mimics-adductor-enthesopathy
#17
Y M Zheng, W Z Li, Z X Wang, W Zhang, H Lv, J X Xiao, Y Yuan
OBJECTIVE: To report thigh muscle magnetic resonance imaging (MRI) tests of four Chinese patients with dystrophinopathy with edema changes in adductor longus muscles that mimics adductor enthesopathy. METHODS: Four boys, who were from four unrelated families and aged from 5 to 11 years, were investigated because of the clinical manifestations including myalgia or muscle weakness or the incidental findings of elevated serum creatine kinase levels, and were diagnosed with dystrophinopathy by gene test of Duchenne muscular dystrophy (DMD)...
October 18, 2016: Beijing da Xue Xue Bao. Yi Xue Ban, Journal of Peking University. Health Sciences
https://www.readbyqxmd.com/read/27744317/dux4-induces-a-transcriptome-more-characteristic-of-a-less-differentiated-cell-state-and-inhibits-myogenesis
#18
Paul Knopp, Yvonne D Krom, Christopher R S Banerji, Maryna Panamarova, Louise A Moyle, Bianca den Hamer, Silvère M van der Maarel, Peter S Zammit
Skeletal muscle wasting in facioscapulohumeral muscular dystrophy (FSHD) results in substantial morbidity. On a disease-permissive chromosome 4qA haplotype, genomic and/or epigenetic changes at the D4Z4 macrosatellite repeat allows transcription of the DUX4 retrogene. Analysing transgenic mice carrying a human D4Z4 genomic locus from an FSHD-affected individual showed that DUX4 was transiently induced in myoblasts during skeletal muscle regeneration. Centromeric to the D4Z4 repeats is an inverted D4Z4 unit encoding DUX4c...
October 15, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27734557/small-fractions-of-muscular-dystrophy-embryonic-stem-cells-yield-severe-cardiac-and-skeletal-muscle-defects-in-adult-mouse-chimeras
#19
J Patrick Gonzalez, Sergii Kyrychenko, Viktoriia Kyrychenko, Joel S Schneider, Celine J Granier, Eric Himelman, Kevin C Lahey, Qingshi Zhao, Ghassan Yehia, Yuan-Xiang Tao, Mantu Bhaumik, Natalia Shirokova, Diego Fraidenraich
Duchenne muscular dystrophy (DMD) is characterized by the loss of the protein dystrophin, leading to muscle fragility, progressive weakening, and susceptibility to mechanical stress. Although dystrophin-negative mdx mouse models have classically been used to study DMD, phenotypes appear mild compared to patients. As a result, characterization of muscle pathology, especially in the heart, has proven difficult. We report that injection of mdx embryonic stem cells (ESCs) into Wild Type blastocysts produces adult mouse chimeras with severe DMD phenotypes in the heart and skeletal muscle...
October 13, 2016: Stem Cells
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
#20
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
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