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Skeletal muscle damage

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https://www.readbyqxmd.com/read/29452783/oxidative-stress-is-increased-in-sarcopenia-and-associated-with-cardiovascular-disease-risk-in-sarcopenic-obesity
#1
Francesco Bellanti, Antonino D Romano, Aurelio Lo Buglio, Valeria Castriotta, Giuseppe Guglielmi, Antonio Greco, Gaetano Serviddio, Gianluigi Vendemiale
OBJECTIVES: To define whether circulating markers of oxidative stress correlate with sarcopenia in terms of glutathione balance and oxidative protein damage, and whether these biomarkers are associated with risk of cardiovascular disease (CVD). STUDY DESIGN: Population-based cross-sectional study. 115 out of 347 elderly subjects were classified as non-sarcopenic non-obese (NS-NO), sarcopenic non-obese (S-NO), non-sarcopenic obese (NS-O), and sarcopenic obese (S-O)...
March 2018: Maturitas
https://www.readbyqxmd.com/read/29448197/pi3k-akt-signaling-pathway-involvement-in-fluoride-induced-apoptosis-in-c2c12-cells
#2
Bian-Hua Zhou, Pan-Pan Tan, Liu-Shu Jia, Wen-Peng Zhao, Ji-Cang Wang, Hong-Wei Wang
To investigate the mechanisms of fluoride-induced apoptosis, a fluoride-induced C2C12 skeletal muscle cell (C2C12 cell) model was established in this study, and the viability of the C2C12 cells was measured using an MTT assay. Cell morphological changes were observed via haematoxylin and eosin staining and transmission electron microscopy. Apoptosis was monitored through Hoechst staining. The mRNA and protein expression of PI3K, PDK1, AKT1, BAD, Bcl-2, Bax and caspase-9 were detected through real-time PCR and western blotting, respectively...
February 9, 2018: Chemosphere
https://www.readbyqxmd.com/read/29444715/porcine-wharton-s-jelly-cells-distribute-throughout-the-body-after-intraperitoneal-injection
#3
Kreeson Packthongsuk, Theresa Rathbun, Deryl Troyer, Duane L Davis
BACKGROUND: Wharton's jelly cells (WJCs) have multiple differentiation potentials and are easily harvested in large numbers. WJCs are well tolerated in allogeneic environments and there is a growing list of their therapeutic effects. Most therapies require administering large numbers of cells and this is generally accomplished by intravenous injection. Here, we studied the locations of porcine WJCs in immune-competent, allogeneic hosts after intraperitoneal (IP) injection. METHODS: Male porcine WJCs were administered to female neonatal piglets by IP injection...
February 14, 2018: Stem Cell Research & Therapy
https://www.readbyqxmd.com/read/29444710/a-novel-in-vitro-model-for-the-assessment-of-postnatal-myonuclear-accretion
#4
Anita Kneppers, Lex Verdijk, Chiel de Theije, Mark Corten, Ellis Gielen, Luc van Loon, Annemie Schols, Ramon Langen
BACKGROUND: Due to the post-mitotic nature of myonuclei, postnatal myogenesis is essential for skeletal muscle growth, repair, and regeneration. This process is facilitated by satellite cells through proliferation, differentiation, and subsequent fusion with a pre-existing muscle fiber (i.e., myonuclear accretion). Current knowledge of myogenesis is primarily based on the in vitro formation of syncytia from myoblasts, which represents aspects of developmental myogenesis, but may incompletely portray postnatal myogenesis...
February 14, 2018: Skeletal Muscle
https://www.readbyqxmd.com/read/29434825/changes-in-inflammatory-and-oxidative-stress-factors-and-the-protein-synthesis-pathway-in-injured-skeletal-muscle-after-contusion
#5
Xiaoguang Liu, Zhigang Zeng, Linlin Zhao, Weihua Xiao, Peijie Chen
Injury of skeletal muscle, and particularly mechanically-induced damage, including contusion injury, frequently occurs in contact sports as well as in sports with accidental contact. Although the mechanisms of skeletal muscle regeneration are well understood, those involved in muscle contusion are not. A total of 40 male mice were randomly divided into control (n=8) and muscle contusion (n=32) groups. A muscle contusion model was established by weight-drop injury. Subsequently, the gastrocnemius muscles in the two groups were harvested at different times (1, 3, 7 and 14 days) post-injury...
February 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29420541/genetic-compensation-triggered-by-actin-mutation-prevents-the-muscle-damage-caused-by-loss-of-actin-protein
#6
Tamar E Sztal, Emily A McKaige, Caitlin Williams, Avnika A Ruparelia, Robert J Bryson-Richardson
The lack of a mutant phenotype in homozygous mutant individuals' due to compensatory gene expression triggered upstream of protein function has been identified as genetic compensation. Whilst this intriguing process has been recognized in zebrafish, the presence of homozygous loss of function mutations in healthy human individuals suggests that compensation may not be restricted to this model. Loss of skeletal ∞-actin results in nemaline myopathy and we have previously shown that the pathological symptoms of the disease and reduction in muscle performance are recapitulated in a zebrafish antisense morpholino knockdown model...
February 8, 2018: PLoS Genetics
https://www.readbyqxmd.com/read/29419410/fat-in-the-blood-fat-in-the-artery-fat-in-the-heart-triglyceride-in-physiology-and-disease
#7
REVIEW
Ira J Goldberg
Cholesterol is not the only lipid that causes heart disease. Triglyceride supplies the heart and skeletal muscles with highly efficient fuel and allows for the storage of excess calories in adipose tissue. Failure to transport, acquire, and use triglyceride leads to energy deficiency and even death. However, overabundance of triglyceride can damage and impair tissues. Circulating lipoprotein-associated triglycerides are lipolyzed by lipoprotein lipase (LpL) and hepatic triglyceride lipase. We inhibited these enzymes and showed that LpL inhibition reduces high-density lipoprotein cholesterol by >50%, and hepatic triglyceride lipase inhibition shifts low-density lipoprotein to larger, more buoyant particles...
February 1, 2018: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29412689/branched-fibers-from-old-fast-twitch-dystrophic-muscles-are-the-sites-of-terminal-damage-in-muscular-dystrophy
#8
Leonit Kiriaev, Sindy Kueh, John W Morley, Kathryn N North, Peter J Houweling, Stewart I Head
A striking pathological feature of dystrophinopathies is the presence of morphologically abnormal branched skeletal muscle fibers. The deterioration of muscle contractile function in Duchenne muscular dystrophy is accompanied by both an increase in number and complexity of these branched fibers. We propose that when number and complexity of branched fibers reaches a critical threshold, "tipping point" the branches in and of themselves are the site of contraction-induced rupture. In the present study, we use the dystrophic mdx mouse and littermate controls to study the pre-diseased dystrophic fast-twitch EDL muscle at 2-3-weeks, the peak myonecrotic phase at 6-9 weeks and finally "old" at 58-112 weeks...
February 7, 2018: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29410655/macrod1-is-a-promiscuous-adp-ribosyl-hydrolase-localized-to-mitochondria
#9
Thomas Agnew, Deeksha Munnur, Kerryanne Crawford, Luca Palazzo, Andreja Mikoč, Ivan Ahel
MacroD1 is a macrodomain containing protein that has mono-ADP-ribose hydrolase enzymatic activity toward several ADP-ribose adducts. Dysregulation of MacroD1 expression has been shown to be associated with the pathogenesis of several forms of cancer. To date, the physiological functions and sub-cellular localization of MacroD1 are unclear. Previous studies have described nuclear and cytosolic functions of MacroD1. However, in this study we show that endogenous MacroD1 protein is highly enriched within mitochondria...
2018: Frontiers in Microbiology
https://www.readbyqxmd.com/read/29408692/proteomic-analysis-of-the-sarcolemma-enriched-fraction-from-dystrophic-mdx-4cv-skeletal-muscle
#10
Sandra Murphy, Margit Zweyer, Michael Henry, Paula Meleady, Rustam R Mundegar, Dieter Swandulla, Kay Ohlendieck
The highly progressive neuromuscular disorder dystrophinopathy is triggered by primary abnormalities in the Dmd gene, which causes cytoskeletal instability and loss of sarcolemmal integrity. Comparative organellar proteomics was employed to identify sarcolemma-associated proteins with an altered concentration in dystrophic muscle tissue from the mdx-4cv mouse model of dystrophinopathy. A lectin agglutination method was used to prepare a sarcolemma-enriched fraction and resulted in the identification of 190 significantly changed protein species...
February 1, 2018: Journal of Proteomics
https://www.readbyqxmd.com/read/29408301/bradykinin-mediates-myogenic-differentiation-in-murine-myoblasts-through-the-involvement-of-sk1-spns2-s1p2-axis
#11
Gennaro Bruno, Francesca Cencetti, Caterina Bernacchioni, Chiara Donati, Kira Vanessa Blankenbach, Dominique Thomas, Dagmar Meyer Zu Heringdorf, Paola Bruni
Skeletal muscle tissue retains a remarkable regenerative capacity due to the activation of resident stem cells that in pathological conditions or after tissue damage proliferate and commit themselves into myoblasts. These immature myogenic cells undergo differentiation to generate new myofibers or repair the injured ones, giving a strong contribution to muscle regeneration. Cytokines and growth factors, potently released after tissue injury by leukocytes and macrophages, are not only responsible of the induction of the initial inflammatory response, but can also affect skeletal muscle regeneration...
February 2, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29404727/combined-use-of-bone-marrow-derived-mesenchymal-stromal-cells-bm-mscs-and-platelet-rich-plasma-prp-stimulates-proliferation-and-differentiation-of-myoblasts-in-vitro-new-therapeutic-perspectives-for-skeletal-muscle-repair-regeneration
#12
Chiara Sassoli, Larissa Vallone, Alessia Tani, Flaminia Chellini, Daniele Nosi, Sandra Zecchi-Orlandini
Satellite cell-mediated skeletal muscle repair/regeneration is compromised in cases of extended damage. Bone marrow mesenchymal stromal cells (BM-MSCs) hold promise for muscle healing but some criticisms hamper their clinical application, including the need to avoid animal serum contamination for expansion and the scarce survival after transplant. In this context, platelet-rich plasma (PRP) could offer advantages. Here, we compare the effects of PRP or standard culture media on C2C12 myoblast, satellite cell and BM-MSC viability, survival, proliferation and myogenic differentiation and evaluate PRP/BM-MSC combination effects in promoting myogenic differentiation...
February 5, 2018: Cell and Tissue Research
https://www.readbyqxmd.com/read/29396483/contractile-skeletal-muscle-cells-cultured-with-a-conducting-soft-wire-for-effective-selective-stimulation
#13
Kuniaki Nagamine, Hirotaka Sato, Hiroyuki Kai, Hirokazu Kaji, Makoto Kanzaki, Matsuhiko Nishizawa
Contractile skeletal muscle cells were cultured so as to wrap around an electrode wire to enable their selective stimulation even when they were co-cultured with other electrically-excitable cells. Since the electrode wire was composed of the conducting polymer poly(3,4-ethylenedioxythiophene) (PEDOT) and polyurethane (PU), which is soft and highly capacitive (~10 mF cm-2), non-faradaic electrical stimulation with charge/discharge currents could be applied to the surrounding cells without causing significant damage even for longer periods (more than a week)...
February 2, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29395744/tourniquet-time-in-total-knee-arthroplasty
#14
Lasse E Rasmussen, Henriette A Holm, Per W Kristensen, Per Kjaersgaard-Andersen
BACKGROUND: Whether the arterial tourniquet in total knee arthroplasty (TKA) is a friend or a foe is still debated. Longer ischemia causes hypoxic damage; yet short duration of a tourniquet may influence outcome. Understanding the time-dependent influence of the tourniquet in TKA patients could improve the overall outcome and safety. The purpose of the study was to measure the tourniquet-induced time-dependent alterations in skeletal muscle metabolism in TKA to establish a 'safe tourniquet time...
January 26, 2018: Knee
https://www.readbyqxmd.com/read/29395054/inhibition-of-methyltransferase-setd7-allows-the-in-vitro-expansion-of-myogenic-stem-cells-with-improved-therapeutic-potential
#15
Robert N Judson, Marco Quarta, Menno J Oudhoff, Hesham Soliman, Lin Yi, Chih Kai Chang, Gloria Loi, Ryan Vander Werff, Alissa Cait, Mark Hamer, Justin Blonigan, Patrick Paine, Linda T N Doan, Elena Groppa, WenJun He, Le Su, Regan H Zhang, Peter Xu, Christine Eisner, Marcela Low, Ingrid Barta, Coral-Ann B Lewis, Colby Zaph, Mohammad M Karimi, Thomas A Rando, Fabio M Rossi
The development of cell therapy for repairing damaged or diseased skeletal muscle has been hindered by the inability to significantly expand immature, transplantable myogenic stem cells (MuSCs) in culture. To overcome this limitation, a deeper understanding of the mechanisms regulating the transition between activated, proliferating MuSCs and differentiation-primed, poorly engrafting progenitors is needed. Here, we show that methyltransferase Setd7 facilitates such transition by regulating the nuclear accumulation of β-catenin in proliferating MuSCs...
February 1, 2018: Cell Stem Cell
https://www.readbyqxmd.com/read/29394360/the-roles-of-muscle-stem-cells-in-muscle-injury-atrophy-and-hypertrophy
#16
So-Ichiro Fukada
Skeletal muscle is composed of multinuclear cells called myofibers. Muscular dystrophy (a genetic muscle disorder) induces instability in the cell membrane of myofibers and eventually causes myofiber damage. Non-genetic muscle disorders, including sarcopenia, diabetes, bedridden immobility, and cancer cachexia, lead to atrophy of myofibers. In contrast, resistance training induces myofiber hypertrophy. Thus, myofibers exhibit a plasticity that is strongly affected by both intrinsic and extrinsic factors. There is no doubt that muscle stem cells (MuSCs, also known as muscle satellite cells) are indispensable for muscle repair/regeneration, but their contributions to atrophy and hypertrophy are still controversial...
January 31, 2018: Journal of Biochemistry
https://www.readbyqxmd.com/read/29385043/interplay-between-ros-and-antioxidants-during-ischemia-reperfusion-injuries-in-cardiac-and-skeletal-muscle
#17
REVIEW
Tingyang Zhou, Evan R Prather, Davis E Garrison, Li Zuo
Ischemia reperfusion (IR), present in myocardial infarction or extremity injuries, is a major clinical issue and leads to substantial tissue damage. Molecular mechanisms underlying IR injury in striated muscles involve the production of reactive oxygen species (ROS). Excessive ROS accumulation results in cellular oxidative stress, mitochondrial dysfunction, and initiation of cell death by activation of the mitochondrial permeability transition pore. Elevated ROS levels can also decrease myofibrillar Ca2+ sensitivity, thereby compromising muscle contractile function...
January 31, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29380956/polyphenol-supplementation-alters-intramuscular-apoptotic-signaling-following-acute-resistance-exercise
#18
Jeremy R Townsend, Jeffrey R Stout, Adam R Jajtner, David D Church, Kyle S Beyer, Joshua J Riffe, Tyler W D Muddle, Kelli L Herrlinger, David H Fukuda, Jay R Hoffman
The purpose of this study was to examine the effects of 28-days of supplementation with an aqueous proprietary polyphenol blend (PPB) sourced from Camellia sinensis on intramuscular apoptotic signaling following an acute lower-body resistance exercise protocol and subsequent recovery. Untrained males (n = 38, 21.8 ± 2.7 years, 173.4 ± 7.9 cm, 77.6 ± 14.6 kg) were randomized to PPB (n = 14), placebo (PL; n = 14) or control (CON; n = 10). Participants completed a lower-body resistance exercise protocol comprised of the squat, leg press, and leg extension exercises...
January 2018: Physiological Reports
https://www.readbyqxmd.com/read/29371959/modulating-the-metabolism-by-trimetazidine-enhances-myoblast-differentiation-and-promotes-myogenesis-in-cachectic-tumor-bearing-c26-mice
#19
Lucia Gatta, Laura Vitiello, Stefania Gorini, Sergio Chiandotto, Paola Costelli, Anna Maria Giammarioli, Walter Malorni, Giuseppe Rosano, Elisabetta Ferraro
Trimetazidine (TMZ) is a metabolic reprogramming agent able to partially inhibit mitochondrial free fatty acid β-oxidation while enhancing glucose oxidation. Here we have found that the metabolic shift driven by TMZ enhances the myogenic potential of skeletal muscle progenitor cells leading to MyoD, Myogenin, Desmin and the slow isoforms of troponin C and I over-expression. Moreover, similarly to exercise, TMZ stimulates the phosphorylation of the AMP-activated protein kinase (AMPK) and up-regulates the peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α), both of which are known to enhance the mitochondrial biogenesis necessary for myoblast differentiation...
December 26, 2017: Oncotarget
https://www.readbyqxmd.com/read/29371665/lsd1-regulates-skeletal-muscle-regeneration-and-directs-the-fate-of-satellite-cells
#20
Milica Tosic, Anita Allen, Dominica Willmann, Christoph Lepper, Johnny Kim, Delphine Duteil, Roland Schüle
Satellite cells are muscle stem cells required for muscle regeneration upon damage. Of note, satellite cells are bipotent and have the capacity to differentiate not only into skeletal myocytes, but also into brown adipocytes. Epigenetic mechanisms regulating fate decision and differentiation of satellite cells during muscle regeneration are not yet fully understood. Here, we show that elevated levels of lysine-specific demethylase 1 (Kdm1a, also known as Lsd1) have a beneficial effect on muscle regeneration and recovery after injury, since Lsd1 directly regulates key myogenic transcription factor genes...
January 25, 2018: Nature Communications
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