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Muscular Regeneration

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https://www.readbyqxmd.com/read/29224095/sex-differences-in-muscle-wasting
#1
Lindsey J Anderson, Haiming Liu, Jose M Garcia
With aging and other muscle wasting diseases, men and women undergo similar pathological changes in skeletal muscle: increased inflammation, enhanced oxidative stress, mitochondrial dysfunction, satellite cell senescence, elevated apoptosis and proteasome activity, and suppressed protein synthesis and myocyte regeneration. Decreased food intake and physical activity also indirectly contribute to muscle wasting. Sex hormones also play important roles in maintaining skeletal muscle homeostasis. Testosterone is a potent anabolic factor promoting muscle protein synthesis and muscular regeneration...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29223663/patch-esophagoplasty-using-an-in-body-tissue-engineered-collagenous-connective-tissue-membrane
#2
Hiroomi Okuyama, Satoshi Umeda, Yuichi Takama, Takeshi Terasawa, Yasuhide Nakayama
AIM: Although many approaches to esophageal replacement have been investigated, these efforts have thus far only met limited success. In-body-tissue-engineered connective tissue tubes have been reported to be effective as vascular replacement grafts. The aim of this study was to investigate the usefulness of an In-body-tissue-engineered collagenous connective tissue membrane, "Biosheet", as a novel esophageal scaffold in a beagle model. METHODS: We prepared Biosheets by embedding specially designed molds into subcutaneous pouches in beagles...
November 13, 2017: Journal of Pediatric Surgery
https://www.readbyqxmd.com/read/29215066/pharmacological-inhibition-of-rev-erb-stimulates-differentiation-inhibits-turnover-and-reduces-fibrosis-in-dystrophic-muscle
#3
Ryan D Welch, Cyrielle Billon, Aurore-Cecile Valfort, Thomas P Burris, Colin A Flaveny
Duchenne muscular dystrophy (DMD) is a debilitating X-linked disorder that is fatal. DMD patients lack the expression of the structural protein dystrophin caused by mutations within the DMD gene. The absence of functional dystrophin protein results in excessive damage from normal muscle use due to the compromised structural integrity of the dystrophin associated glycoprotein complex. As a result, DMD patients exhibit ongoing cycles of muscle destruction and regeneration that promote inflammation, fibrosis, mitochondrial dysfunction, satellite cell (SC) exhaustion and loss of skeletal and cardiac muscle function...
December 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29211034/glucocorticoids-improve-myogenic-differentiation-in-vitro-by-suppressing-the-synthesis-of-versican-a-transitional-matrix-protein-overexpressed-in-dystrophic-skeletal-muscles
#4
Natasha McRae, Leonard Forgan, Bryony McNeill, Alex Addinsall, Daniel McCulloch, Chris Van der Poel, Nicole Stupka
In Duchenne muscular dystrophy (DMD), a dysregulated extracellular matrix (ECM) directly exacerbates pathology. Glucocorticoids are beneficial therapeutics in DMD, and have pleiotropic effects on the composition and processing of ECM proteins in other biological contexts. The synthesis and remodelling of a transitional versican-rich matrix is necessary for myogenesis; whether glucocorticoids modulate this transitional matrix is not known. Here, versican expression and processing were examined in hindlimb and diaphragm muscles from mdx dystrophin-deficient mice and C57BL/10 wild type mice...
December 6, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29203713/therapeutic-potential-of-heat-shock-protein-induction-for-muscular-dystrophy-and-other-muscle-wasting-conditions
#5
REVIEW
Savant S Thakur, Kristy Swiderski, James G Ryall, Gordon S Lynch
Duchenne muscular dystrophy is the most common and severe of the muscular dystrophies, a group of inherited myopathies caused by different genetic mutations leading to aberrant expression or complete absence of cytoskeletal proteins. Dystrophic muscles are prone to injury, and regenerate poorly after damage. Remorseless cycles of muscle fibre breakdown and incomplete repair lead to progressive and severe muscle wasting, weakness and premature death. Many other conditions are similarly characterized by muscle wasting, including sarcopenia, cancer cachexia, sepsis, denervation, burns, and chronic obstructive pulmonary disease...
January 19, 2018: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
https://www.readbyqxmd.com/read/29194448/interleukin-1beta-il-1%C3%AE-induced-notch-ligand-jagged1-suppresses-mitogenic-action-of-il-1%C3%AE-on-human-dystrophic-myogenic-cells
#6
Yuki Nagata, Tohru Kiyono, Kikuo Okamura, Yu-Ichi Goto, Masafumi Matsuo, Madoka Ikemoto-Uezumi, Naohiro Hashimoto
Duchenne muscular dystrophy (DMD) is a severe X-linked recessive muscle disorder caused by mutations in the dystrophin gene. Nonetheless, secondary processes involving perturbation of muscle regeneration probably exacerbate disease progression, resulting in the fatal loss of muscle in DMD patients. A dysfunction of undifferentiated myogenic cells is the most likely cause for the reduction of regenerative capacity of muscle. To clarify molecular mechanisms in perturbation of the regenerative capacity of DMD muscle, we have established several NCAM (CD56)-positive immortalized human dystrophic and non-dystrophic myogenic cell lines from DMD and healthy muscles...
2017: PloS One
https://www.readbyqxmd.com/read/29192166/spindle-associated-membrane-protein-1-samp1-is-required-for-the-differentiation-of-muscle-cells
#7
Mohammed Hakim Jafferali, Ricardo A Figueroa, Mehedi Hasan, Einar Hallberg
Muscles are developed and regenerated in a differentiation process called myogenesis, which involves components of the nuclear envelope. We have investigated Samp1 (Spindle Associated Membrane Protein 1), a transmembrane nuclear envelope protein, which interacts with emerin and lamin A, both of which are linked to Emery-Dreifuss muscular dystrophy (EDMD). We found that the levels of Samp1 increased seven-fold during differentiation of mouse C2C12 muscle progenitor cells. To test if Samp1 could have a role in myogenesis we developed stable C2C12 knockdown cell lines expressing short hairpin RNA targeting Samp1 expression...
November 30, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29183282/bilateral-muscle-fiber-and-nerve-influences-by-tnf-alpha-in-response-to-unilateral-muscle-overuse-studies-on-tnf-receptor-expressions
#8
Lina Renström, Per Stål, Yafeng Song, Sture Forsgren
BACKGROUND: TNF-alpha is suggested to be involved in muscle damage and muscle inflammation (myositis). In order to evaluate whether TNF-alpha is involved in the myositis that occurs in response to muscle overuse, the aim was to examine the expression patterns of TNF receptors in this condition. METHODS: A rabbit muscle overuse model leading to myositis in the soleus muscle was used. The expression patterns of the two TNF receptors Tumor Necrosis Factor Receptor type 1 (TNFR1) and Tumor Necrosis Factor Receptor type 2 (TNFR2) were investigated...
November 28, 2017: BMC Musculoskeletal Disorders
https://www.readbyqxmd.com/read/29163212/regulation-of-skeletal-muscle-plasticity-by-protein-arginine-methyltransferases-and-their-potential-roles-in-neuromuscular-disorders
#9
REVIEW
Derek W Stouth, Tiffany L vanLieshout, Nicole Y Shen, Vladimir Ljubicic
Protein arginine methyltransferases (PRMTs) are a family of enzymes that catalyze the methylation of arginine residues on target proteins, thereby mediating a diverse set of intracellular functions that are indispensable for survival. Indeed, full-body knockouts of specific PRMTs are lethal and PRMT dysregulation has been implicated in the most prevalent chronic disorders, such as cancers and cardiovascular disease (CVD). PRMTs are now emerging as important mediators of skeletal muscle phenotype and plasticity...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/29157305/evaluation-of-the-effect-of-a-floxed-neo-cassette-within-the-dystroglycan-dag1-gene
#10
Francesca Sciandra, Bianca Maria Scicchitano, Giulia Signorino, Maria Giulia Bigotti, Barbara Tavazzi, Francesca Lombardi, Manuela Bozzi, Gigliola Sica, Bruno Giardina, Sandra Blaess, Andrea Brancaccio
OBJECTIVE: Dystroglycan (DG) is an adhesion complex formed by two subunits, α-DG and β-DG. In skeletal muscle, DG is part of the dystrophin-glycoprotein complex that is crucial for sarcolemma stability and it is involved in a plethora of muscular dystrophy phenotypes. Due to the important role played by DG in skeletal muscle stability as well as in a wide variety of other tissues including brain and the peripheral nervous system, it is essential to investigate its genetic assembly and transcriptional regulation...
November 21, 2017: BMC Research Notes
https://www.readbyqxmd.com/read/29123500/efficacy-and-the-safety-of-granulocyte-colony-stimulating-factor-treatment-in-patients-with-muscular-dystrophy-a-non-randomized-clinical-trial
#11
Dorota Sienkiewicz, Wojciech Kułak, Bożena Okurowska-Zawada, Grażyna Paszko-Patej, Janusz Wojtkowski, Karolina Sochoń, Anna Kalinowska, Kamila Okulczyk, Jerzy Sienkiewicz, Edward McEachern
Introduction: The current standard treatment for patients with Duchenne muscular dystrophy (DMD) involves corticosteroids. Granulocyte colony-stimulating factor (G-CSF) induces the proliferation of satellite cells and myoblasts and, in turn, muscle regeneration. Beneficial effects of G-CSF were also described for skeletal muscle disorders. Aim: We assessed the safety and effects of using G-CSF to promote muscle strength in patients with DMD. Materials and methods: Inclusion criteria were as follows: patients aged 5-15 years with diagnosed with DMD confirmed by genetic test or biopsy...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/29111336/regenerative-effects-of-basic-fibroblast-growth-factor-on-restoration-of-thyroarytenoid-muscle-atrophy-caused-by-recurrent-laryngeal-nerve-transection
#12
Mami Kaneko, Takuya Tsuji, Yo Kishimoto, Yoichiro Sugiyama, Tatsuo Nakamura, Shigeru Hirano
OBJECTIVES: Vocal fold atrophy following unilateral vocal fold paralysis is caused by atrophy of the thyroarytenoid (TA) muscle and remains a challenge. Medialization procedures are popular treatment options; however, hoarseness often remains due to the reduction in mass or tension of the TA muscle. Therefore, in addition to medialization procedures, TA muscle reinnervation is desirable. In vivo studies have shown the potential for basic fibroblast growth factor (bFGF) to affect muscular and nerve regeneration...
October 27, 2017: Journal of Voice: Official Journal of the Voice Foundation
https://www.readbyqxmd.com/read/29101541/rotator-cuff-muscular-integrity-after-arthroscopic-revision-of-a-bankart-repair
#13
Johannes Buckup, Frederic Welsch, Reinhard Hoffmann, Philip P Roessler, Karl F Schüttler, Thomas Stein
INTRODUCTION: Recurrent shoulder instability after arthroscopic Bankart repair is still a common complication. For primary Bankart repair studies have shown that the rotator cuff can recover completely. The ability of muscles to regenerate after arthroscopic revision Bankart repair (ARBR) has not been studied. Does the ARBR using a three-portal method allows complete muscle integrity compared with an uninjured imaging control group (ICG)? MATERIALS AND METHODS: Twenty-two (1 female, 21 males) physically active patients (mean age at follow-up 28...
November 3, 2017: Archives of Orthopaedic and Trauma Surgery
https://www.readbyqxmd.com/read/29093487/micrornas-promote-skeletal-muscle-differentiation-of-mesodermal-ipsc-derived-progenitors
#14
Giorgia Giacomazzi, Bryan Holvoet, Sander Trenson, Ellen Caluwé, Bojana Kravic, Hanne Grosemans, Álvaro Cortés-Calabuig, Christophe M Deroose, Danny Huylebroeck, Said Hashemolhosseini, Stefan Janssens, Elizabeth McNally, Mattia Quattrocelli, Maurilio Sampaolesi
Muscular dystrophies (MDs) are often characterized by impairment of both skeletal and cardiac muscle. Regenerative strategies for both compartments therefore constitute a therapeutic avenue. Mesodermal iPSC-derived progenitors (MiPs) can regenerate both striated muscle types simultaneously in mice. Importantly, MiP myogenic propensity is influenced by somatic lineage retention. However, it is still unknown whether human MiPs have in vivo potential. Furthermore, methods to enhance the intrinsic myogenic properties of MiPs are likely needed, given the scope and need to correct large amounts of muscle in the MDs...
November 1, 2017: Nature Communications
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
#15
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/29068540/the-molecular-cross-talk-of-the-dystrophin-glycoprotein-complex
#16
REVIEW
Marta Gawor, Tomasz J Prószyński
The proper function of skeletal muscles relies on their ability to process signals derived from motor neurons, transmit stimuli along the muscle fibers, contract, and regenerate efficiently after injury. The dystrophin-glycoprotein complex (DGC; also called the dystrophin-associated protein complex) plays a central role in all of these processes. It acts as a transmembrane platform that anchors the extracellular matrix (ECM) to the intracellular cytoskeleton and makes muscle fibers more resistant to injury...
October 25, 2017: Annals of the New York Academy of Sciences
https://www.readbyqxmd.com/read/29067668/advanced-methods-to-study-the-cross-talk-between-fibro-adipogenic-progenitors-and-muscle-stem-cells
#17
Luca Tucciarone, Usue Etxaniz, Martina Sandoná, Silvia Consalvi, Pier Lorenzo Puri, Valentina Saccone
Functional interactions between muscle (satellite) stem cells-MuSCs-and other cellular components of their niche (the fibro-adipogenic progenitors-FAPs) coordinate regeneration of injured as well as diseased skeletal muscles. These interactions are largely mediated by secretory networks, whose integrity is critical to determine whether repair occurs by compensatory regeneration leading to formation of new contractile fibers, or by maladaptive formation of fibrotic scars and fat infiltration. Here we provide the description of methods for isolation of FAPs and MuSCs from muscles of wild type and dystrophic mice, and protocols of cocultures as well as MuSC's exposure to FAP- derived exosomes...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29067655/characterization-of-the-inflammatory-response-in-dystrophic-muscle-using-flow-cytometry
#18
Jenna M Kastenschmidt, Ileen Avetyan, S Armando Villalta
Although mutations of the dystrophin gene are the causative defect in Duchenne muscular dystrophy (DMD) patients, secondary disease processes such as inflammation contribute greatly to the pathogenesis of DMD. Genetic and histological studies have shown that distinct facets of the immune system promote muscle degeneration or regeneration during muscular dystrophy through mechanisms that are only beginning to be defined. Although histological methods have allowed the enumeration and localization of immune cells within dystrophic muscle, they are limited in their ability to assess the full spectrum of phenotypic states of an immune cell population and its functional characteristics...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29057908/silencing-nfix-rescues-muscular-dystrophy-by-delaying-muscle-regeneration
#19
Giuliana Rossi, Chiara Bonfanti, Stefania Antonini, Mattia Bastoni, Stefania Monteverde, Anna Innocenzi, Marielle Saclier, Valentina Taglietti, Graziella Messina
Muscular dystrophies are severe disorders due to mutations in structural genes, and are characterized by skeletal muscle wasting, compromised patient mobility, and respiratory functions. Although previous works suggested enhancing regeneration and muscle mass as therapeutic strategies, these led to no long-term benefits in humans. Mice lacking the transcription factor Nfix have delayed regeneration and a shift toward an oxidative fiber type. Here, we show that ablating or silencing the transcription factor Nfix ameliorates pathology in several forms of muscular dystrophy...
October 20, 2017: Nature Communications
https://www.readbyqxmd.com/read/29051551/reducing-sarcolipin-expression-mitigates-duchenne-muscular-dystrophy-and-associated-cardiomyopathy-in-mice
#20
Antanina Voit, Vishwendra Patel, Ronald Pachon, Vikas Shah, Mohammad Bakhutma, Erik Kohlbrenner, Joseph J McArdle, Louis J Dell'Italia, Jerry R Mendell, Lai-Hua Xie, Roger J Hajjar, Dongsheng Duan, Diego Fraidenraich, Gopal J Babu
Sarcolipin (SLN) is an inhibitor of the sarco/endoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) and is abnormally elevated in the muscle of Duchenne muscular dystrophy (DMD) patients and animal models. Here we show that reducing SLN levels ameliorates dystrophic pathology in the severe dystrophin/utrophin double mutant (mdx:utr (-/-)) mouse model of DMD. Germline inactivation of one allele of the SLN gene normalizes SLN expression, restores SERCA function, mitigates skeletal muscle and cardiac pathology, improves muscle regeneration, and extends the lifespan...
October 20, 2017: Nature Communications
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