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Muscular Regeneration

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
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
Caroline E Brun, Nicolas A Dumont
No abstract text is available yet for this article.
October 2016: Médecine Sciences: M/S
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
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
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
J Patrick Gonzalez, Sergii Kyrychenko, Victoria Kyrychenko, Joel S Schneider, Celine J Granier, Eric Himelman, Kevin 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 (WT) blastocysts produces adult mouse chimeras with severe DMD phenotypes in the heart and skeletal muscle...
October 13, 2016: Stem Cells
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
María Emilia Garcia Denegri, Gladys P Teibler, Silvana L Maruñak, David R Hernández, Ofelia C Acosta, Laura C Leiva
Bothrops alternatus snake venom is particularly characterized for inducing a prominent haemorrhage and affecting hemostasis as a consequence of 43.1% of metallo-proteinases and less than 10% of PLA2 (almost all non-myotoxic phospholipases) in its venomics. In addition, myonecrosis is the major local effect in viper envenoming which might lead to permanent sequela. Then, the rebuilding of the microvasculature at the local injured site acquires significance since represents one of the pivotal stages for subsequent skeletal muscle regeneration either at morphological or functional aspects...
October 6, 2016: Toxicon: Official Journal of the International Society on Toxinology
Ute Ulrike Botzenhart, Constantin Wegenstein, Teodor Todorov, Christiane Kunert-Keil
The most widespread animal model to investigate Duchenne muscular dystrophy is the mdx-mouse. In contrast to humans, phases of muscle degeneration are replaced by regeneration processes; hence there is only a restricted time slot for research. The aim of the study was to investigate if an intramuscular injection of BTX-A is able to break down muscle regeneration and has direct implications on the gene expression of myosin heavy chains in the corresponding treated and untreated muscles. Therefore, paralysis of the right masseter muscle was induced in adult healthy and dystrophic mice by a specific intramuscular injection of BTX-A...
2016: BioMed Research International
Antonio L Serrano, Pura Muñoz-Cánoves
Duchenne muscular dystrophy (DMD) is one of the most devastating neuromuscular genetic diseases caused by the absence of dystrophin. The continuous episodes of muscle degeneration and regeneration in dystrophic muscle are accompanied by chronic inflammation and fibrosis deposition, which exacerbate disease progression. Thus, in addition of investigating strategies to cure the primary defect by gene/cell therapeutic strategies, increasing efforts are being placed on identifying the causes of the substitution of muscle by non-functional fibrotic tissue in DMD, aiming to attenuate its severity...
September 23, 2016: Seminars in Cell & Developmental Biology
George D Bittner, Christopher S Spaeth, Andrew D Poon, Zachary S Burgess, Christopher H McGill
The repair (sealing) of plasmalemmal damage, consisting of small holes to complete transections, is critical for cell survival, especially for neurons that rarely regenerate cell bodies. We first describe and evaluate different measures of cell sealing. Some measures, including morphological/ultra-structural observations, membrane potential, and input resistance, provide very ambiguous assessments of plasmalemmal sealing. In contrast, measures of ionic current flow and dye barriers can, if appropriately used, provide more accurate assessments...
July 2016: Neural Regeneration Research
Rosa Vono, Claudia Fuoco, Stefano Testa, Stefano Pirrò, Davide Maselli, David Ferland Mc Collough, Elena Sangalli, Gianfranco Pintus, Roberta Giordo, Giovanna Finzi, Fausto Sessa, Rosanna Cardani, Ambra Gotti, Sergio Losa, Gianni Cesareni, Roberto Rizzi, Claudia Bearzi, Stefano Cannata, Gaia Spinetti, Cesare Gargioli, Paolo Madeddu
Critical limb ischemia (CLI), foot ulcers, former amputation and impaired regeneration are independent risk factors for limb amputation in diabetic subjects. The present work investigates whether and by which mechanism diabetes negatively impacts on functional properties of muscular pericytes (MPs), which are resident stem cells committed to reparative angiomyogenesis.We obtained muscle biopsies from diabetic patients undergoing major limb amputation and control subjects. Diabetic muscles collected at the rim of normal tissue surrounding the plane of dissection showed myofibres degeneration, fat deposition, and reduction of MPs vascular coverage...
September 6, 2016: Diabetes
Giuseppe Morici, Monica Frinchi, Alessandro Pitruzzella, Valentina Di Liberto, Rosario Barone, Andrea Pace, Valentina Di Felice, Natale Belluardo, Francesco Cappello, Giuseppa Mudò, Maria R Bonsignore
In the mdx mice model of Duchenne Muscular Dystrophy (DMD), mild endurance exercise training positively affected limb skeletal muscles, whereas few and controversial data exist on the effects of training on the diaphragm. The diaphragm was examined in mdx (C57BL/10ScSn-Dmdmdx) and wild type (WT, C57BL/10ScSc) mice under sedentary conditions (mdx-SD, WT-SD) and during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days (training: 5 d/wk for 6 weeks), diaphragm muscle morphology and Cx39 protein were assessed...
August 30, 2016: Journal of Cellular Physiology
Paolo Bettica, Stefania Petrini, Valentina D'Oria, Adele D'Amico, Michela Catteruccia, Marika Pane, Serena Sivo, Francesca Magri, Simona Brajkovic, Sonia Messina, Gian Luca Vita, Barbara Gatti, Maurizio Moggio, Pier Lorenzo Puri, Maurizio Rocchetti, Giuseppe De Nicolao, Giuseppe Vita, Giacomo P Comi, Enrico Bertini, Eugenio Mercuri
Duchenne Muscular Dystrophy (DMD) is caused by mutations in the dystrophin gene leading to dystrophin deficiency, muscle fiber degeneration and progressive fibrotic replacement of muscles. Givinostat, a histone deacetylase (HDAC) inhibitor, significantly reduced fibrosis and promoted compensatory muscle regeneration in mdx mice. This study was conducted to evaluate whether the beneficial histological effects of Givinostat could be extended to DMD boys. Twenty ambulant DMD boys aged 7 to <11 years on stable corticosteroid treatment were enrolled in the study and treated for ≥12 months with Givinostat...
October 2016: Neuromuscular Disorders: NMD
Paul J Thomas, Rui Xu, Paul T Martin
Overexpression of B4GALNT2 (previously GALGT2) inhibits the development of muscle pathology in mouse models of Duchenne muscular dystrophy, congenital muscular dystrophy 1A, and limb girdle muscular dystrophy 2D. In these models, muscle GALGT2 overexpression induces the glycosylation of α dystroglycan with the cytotoxic T cell glycan and increases the overexpression of dystrophin and laminin α2 surrogates known to inhibit disease. Here, we show that GALGT2 gene therapy significantly reduces muscle pathology in FKRP P448Lneo(-) mice, a model for limb girdle muscular dystrophy 2I...
September 2016: American Journal of Pathology
Mona A M Helal, Noura E M Shaheen, Fatma A Abu Zahra
CONTEXT: Cell therapy technique with stem cells is a very attractive strategy for the treatment of muscle disorders. OBJECTIVE: The objective of this study was to investigate the mechanism of local transplantation of mesenchymal stem cells (MSCs) which could contribute to skeletal muscle healing. MATERIALS AND METHODS: Female rats were divided into three equal groups as the following: group 1, the negative control group (untreated group), group 2, sham-treated group, rats with muscle injuries involving volumetric muscle loss (VML) of adductor brevis muscle and injected locally with phosphate-buffered saline (PBS) 0...
August 25, 2016: Immunopharmacology and Immunotoxicology
Agnieszka Kulesza, Anna Burdzinska, Izabela Szczepanska, Weronika Zarychta-Wisniewska, Beata Pajak, Kamil Bojarczuk, Bartosz Dybowski, Leszek Paczek
Both myoblasts and mesenchymal stem cells (MSC) take part in the muscle tissue regeneration and have been used as experimental cellular therapy in muscular disorders treatment. It is possible that co-transplantation approach could improve the efficacy of this treatment. However, the relations between those two cell types are not clearly defined. The aim of this study was to determine the reciprocal interactions between myoblasts and MSC in vitro in terms of the features important for the muscle regeneration process...
2016: PloS One
Jean K Mah
Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy in childhood. It is caused by mutations of the DMD gene, leading to progressive muscle weakness, loss of independent ambulation by early teens, and premature death due to cardiorespiratory complications. The diagnosis can usually be made after careful review of the history and examination of affected boys presenting with developmental delay, proximal weakness, and elevated serum creatine kinase, plus confirmation by muscle biopsy or genetic testing...
2016: Neuropsychiatric Disease and Treatment
Stéphanie Langlois, Kyle N Cowan
Pannexins are newly discovered channels that are now recognized as mediators of adenosine triphosphate release from several cell types allowing communication with the extracellular environment. Pannexins have been associated with various physiological and pathological processes including apoptosis, inflammation, and cancer. However, it is only recently that our work has unveiled a role for Pannexin 1 and Pannexin 3 as novel regulators of skeletal muscle myoblast proliferation and differentiation. Myoblast differentiation is an ordered multistep process that includes withdrawal from the cell cycle and the expression of key myogenic factors leading to myoblast differentiation and fusion into multinucleated myotubes...
August 13, 2016: Advances in Experimental Medicine and Biology
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