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https://www.readbyqxmd.com/read/29783118/placenta-derived-mesenchymal-stromal-cells-and-their-exosomes-exert-therapeutic-effects-in-duchenne-muscular-dystrophy
#1
Ariel Bier, Peter Berenstein, Noam Kronfeld, Daria Morgoulis, Amotz Ziv-Av, Hodaya Goldstein, Gila Kazimirsky, Simona Cazacu, Rinat Meir, Rachela Popovtzer, Amir Dori, Chaya Brodie
Duchenne muscular dystrophy (DMD) is a degenerative lethal, X-linked disease of skeletal and cardiac muscles caused by mutations in the dystrophin gene. Cell therapy using different cell types, including mesenchymal stromal cells (MSCs), has been considered as a potential approach for the treatment of DMD. MSCs can be obtained from autologous sources such as bone marrow and adipose tissues or from allogeneic placenta and umbilical cord. The safety and therapeutic impact of these cells has been demonstrated in pre-clinical and clinical studies and their functions are attributed to paracrine effects that are mediated by secreted cytokines and extracellular vesicles...
May 3, 2018: Biomaterials
https://www.readbyqxmd.com/read/29759937/identification-of-epigenetic-regulators-of-dux4-fl-for-targeted-therapy-of-facioscapulohumeral-muscular-dystrophy
#2
Charis L Himeda, Takako I Jones, Ching-Man Virbasius, Lihua Julie Zhu, Michael R Green, Peter L Jones
Facioscapulohumeral muscular dystrophy (FSHD) is caused by epigenetic de-repression of the disease locus, leading to pathogenic misexpression of the DUX4 gene in skeletal muscle. While the factors and pathways involved in normal repression of the FSHD locus in healthy cells have been well characterized, very little is known about those responsible for the aberrant activation of DUX4-fl in FSHD myocytes. Reasoning that DUX4-fl activators might represent useful targets for small molecule inhibition, we performed a highly targeted, candidate-based screen of epigenetic regulators in primary FSHD myocytes...
April 26, 2018: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/29743983/chemotherapeutic-drugs-and-mitochondrial-dysfunction-focus-on-doxorubicin-trastuzumab-and-sunitinib
#3
REVIEW
Stefania Gorini, Antonella De Angelis, Liberato Berrino, Natalia Malara, Giuseppe Rosano, Elisabetta Ferraro
Many cancer therapies produce toxic side effects whose molecular mechanisms await full elucidation. The most feared and studied side effect of chemotherapeutic drugs is cardiotoxicity. Also, skeletal muscle physiology impairment has been recorded after many chemotherapeutical treatments. However, only doxorubicin has been extensively studied for its side effects on skeletal muscle. Chemotherapeutic-induced adverse side effects are, in many cases, mediated by mitochondrial damage. In particular, trastuzumab and sunitinib toxicity is mainly associated with mitochondria impairment and is mostly reversible...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29743034/glial-cell-line-derived-neurotrophic-factor-gdnf-attenuates-the-peripheral-neuromuscular-dysfunction-without-inhibiting-the-activation-of-spinal-microglia-monocyte
#4
Fei Xie, Fan Zhang, Su Min, Jingyuan Chen, Jun Yang, Xin Wang
BACKGROUND: Peripheral neuromuscular dysfunctions were found in elderly individuals, and spinal microglia/monocyte plays an important role on this process. This study aims to test whether the glial cell line-derived neurotrophic factor (GDNF) could attenuate age-related neuromuscular dysfunction by inhibiting the activation of spinal microglia/monocyte. METHODS: Male Sprague-Dawley rats were divided into an adult group and an aged group. The aged rats were intrathecally injected with normal saline (NS) and GDNF...
May 9, 2018: BMC Geriatrics
https://www.readbyqxmd.com/read/29725254/resveratrol-attenuates-denervation-induced-muscle-atrophy-due-to-the-blockade-of-atrogin-1-and-p62-accumulation
#5
Yuka Asami, Miki Aizawa, Masakazu Kinoshita, Junji Ishikawa, Kunihiro Sakuma
Decrease in activity stress induces skeletal muscle atrophy. A previous study showed that treatment with resveratrol inhibits muscular atrophy in mdx mice, a model of DMD. However, almost all studies using resveratrol supplementation have only looked at adaptive changes in the muscle weight. The present study was designed to elucidate whether the resveratrol-inducing attenuation of skeletal muscle actually reflects the adaptation of muscle fibers themselves, based on the modulation of atrogin-1- or p62-dependent signaling...
2018: International Journal of Medical Sciences
https://www.readbyqxmd.com/read/29703249/mir-708-5p-and-mir-34c-5p-are-involved-in-nnos-regulation-in-dystrophic-context
#6
Marine Guilbaud, Christel Gentil, Cécile Peccate, Elena Gargaun, Isabelle Holtzmann, Carole Gruszczynski, Sestina Falcone, Kamel Mamchaoui, Rabah Ben Yaou, France Leturcq, Laurence Jeanson-Leh, France Piétri-Rouxel
BACKGROUND: Duchenne (DMD) and Becker (BMD) muscular dystrophies are caused by mutations in the DMD gene coding for dystrophin, a protein being part of a large sarcolemmal protein scaffold that includes the neuronal nitric oxide synthase (nNOS). The nNOS was shown to play critical roles in a variety of muscle functions and alterations of its expression and location in dystrophic muscle fiber leads to an increase of the muscle fatigability. We previously revealed a decrease of nNOS expression in BMD patients all presenting a deletion of exons 45 to 55 in the DMD gene (BMDd45-55), impacting the nNOS binding site of dystrophin...
April 27, 2018: Skeletal Muscle
https://www.readbyqxmd.com/read/29700358/premyogenic-progenitors-derived-from-human-pluripotent-stem-cells-expand-in-floating-culture-and-differentiate-into-transplantable-myogenic-progenitors
#7
Fusako Sakai-Takemura, Asako Narita, Satoru Masuda, Toshifumi Wakamatsu, Nobuharu Watanabe, Takashi Nishiyama, Ken'ichiro Nogami, Matthias Blanc, Shin'ichi Takeda, Yuko Miyagoe-Suzuki
Human induced pluripotent stem cells (hiPSCs) are a potential source for cell therapy of Duchenne muscular dystrophy. To reliably obtain skeletal muscle progenitors from hiPSCs, we treated hiPS cells with a Wnt activator, CHIR-99021 and a BMP receptor inhibitor, LDN-193189, and then induced skeletal muscle cells using a previously reported sphere-based culture. This protocol greatly improved sphere formation efficiency and stably induced the differentiation of myogenic cells from hiPS cells generated from both healthy donors and a patient with congenital myasthenic syndrome...
April 26, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29699580/genetic-deletion-of-muscle-rank-or-selective-inhibition-of-rankl-is-not-as-effective-as-full-length-opg-fc-in-mitigating-muscular-dystrophy
#8
Sébastien S Dufresne, Antoine Boulanger-Piette, Sabrina Bossé, Anteneh Argaw, Dounia Hamoudi, Laetitia Marcadet, Daniel Gamu, Val A Fajardo, Hideo Yagita, Josef M Penninger, A Russell Tupling, Jérôme Frenette
Although there is a strong association between osteoporosis and skeletal muscle atrophy/dysfunction, the functional relevance of a particular biological pathway that regulates synchronously bone and skeletal muscle physiopathology is still elusive. Receptor-activator of nuclear factor κB (RANK), its ligand RANKL and the soluble decoy receptor osteoprotegerin (OPG) are the key regulators of osteoclast differentiation and bone remodelling. We thus hypothesized that RANK/RANKL/OPG, which is a key pathway for bone regulation, is involved in Duchenne muscular dystrophy (DMD) physiopathology...
April 24, 2018: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29693488/elevated-tgf-%C3%AE-2-serum-levels-in-emery-dreifuss-muscular-dystrophy-implications-for-myocyte-and-tenocyte-differentiation-and-fibrogenic-processes
#9
Pia Bernasconi, Nicola Carboni, Giulia Ricci, Gabriele Siciliano, Luisa Politano, Lorenzo Maggi, Tiziana Mongini, Liliana Vercelli, Carmelo Rodolico, Elena Biagini, Giuseppe Boriani, Lucia Ruggiero, Lucio Santoro, Elisa Schena, Sabino Prencipe, Camilla Evangelisti, Elena Pegoraro, Lucia Morandi, Marta Columbaro, Chiara Lanzuolo, Patrizia Sabatelli, Paola Cavalcante, Cristina Cappelletti, Gisèle Bonne, Antoine Muchir, Giovanna Lattanzi
Among rare diseases caused by mutations in LMNA gene, Emery-Dreifuss Muscular Dystrophy type 2 and Limb-Girdle muscular Dystrophy 1B are characterized by muscle weakness and wasting, joint contractures, cardiomyopathy with conduction system disorders. Circulating biomarkers for these pathologies have not been identified. Here, we analyzed the secretome of a cohort of patients affected by these muscular laminopathies in the attempt to identify a common signature. Multiplex cytokine assay showed that transforming growth factor beta 2 (TGF β2) and interleukin 17 serum levels are consistently elevated in the vast majority of examined patients, while interleukin 6 and basic fibroblast growth factor are altered in subgroups of patients...
April 25, 2018: Nucleus
https://www.readbyqxmd.com/read/29686622/inhibitory-neural-regulation-of-the-ca-2-transients-in-intramuscular-interstitial-cells-of-cajal-in-the-small-intestine
#10
Salah A Baker, Bernard T Drumm, Caroline A Cobine, Kathleen D Keef, Kenton M Sanders
Gastrointestinal motility is coordinated by enteric neurons. Both inhibitory and excitatory motor neurons innervate the syncytium consisting of smooth muscle cells (SMCs) interstitial cells of Cajal (ICC) and PDGFRα+ cells (SIP syncytium). Confocal imaging of mouse small intestines from animals expressing GCaMP3 in ICC were used to investigate inhibitory neural regulation of ICC in the deep muscular plexus (ICC-DMP). We hypothesized that Ca2+ signaling in ICC-DMP can be modulated by inhibitory enteric neural input...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29672276/blocking-p62-sqstm1-dependent-smn-degradation-ameliorates-spinal-muscular-atrophy-disease-phenotypes
#11
Natalia Rodriguez-Muela, Andrey Parkhitko, Tobias Grass, Rebecca M Gibbs, Erika M Norabuena, Norbert Perrimon, Rajat Singh, Lee L Rubin
Spinal muscular atrophy (SMA), a degenerative motor neuron (MN) disease caused by loss of functional SMN protein due to SMN1 gene mutations, is a leading cause of infant mortality. Increasing SMN levels ameliorates the disease phenotype and is unanimously accepted as a therapeutic approach for SMA patients. The ubiquitin/proteasome system is known to regulate SMN protein levels; however whether autophagy controls SMN levels remains poorly explored. Here we show that SMN protein is degraded by autophagy. Pharmacological and genetic inhibition of autophagy increase SMN levels, while induction of autophagy decreases SMN...
April 19, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29669436/heme-oxygenase-1-influences-satellite-cells-and-progression-of-duchenne-muscular-dystrophy-in-mice
#12
Katarzyna Pietraszek-Gremplewicz, Magdalena Kozakowska, Iwona Bronisz-Budzynska, Maciej Ciesla, Olga Mucha, Paulina Podkalicka, Magdalena Madej, Urszula Glowniak, Krzysztof Tomasz Szade, Jacek Stepniewski, Mateusz Jez, Kalina Andrysiak, Karolina Bukowska-Strakova, Anna Kaminska, Anna Kostera-Pruszczyk, Alicja Jozkowicz, Agnieszka Loboda, Jozef Dulak
AIMS: Muscle damage in Duchenne Muscular Dystrophy (DMD) caused by the lack of dystrophin is strongly linked to inflammation. Heme oxygenase-1 (HO-1; Hmox1) is an anti-inflammatory and cytoprotective enzyme affecting myoblasts differentiation by inhibiting myomirs. The role of HO-1 has not been so far well addressed in DMD. RESULTS: In dystrophin-deficient mdx mice expression of Hmox1 in limb skeletal muscles and diaphragm is higher than in wild-type animals, being consistently elevated from 8 up to 52 weeks, both in myofibres and inflammatory leukocytes...
April 19, 2018: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/29642926/zidovudine-ameliorates-pathology-in-the-mouse-model-of-duchenne-muscular-dystrophy-via-p2rx7-purinoceptor-antagonism
#13
Rasha Al-Khalidi, Chiara Panicucci, Paul Cox, Natalia Chira, Justyna Róg, Christopher N J Young, Rhiannon E McGeehan, Kameshwari Ambati, Jayakrishna Ambati, Krzysztof Zabłocki, Elisabetta Gazzerro, Stephen Arkle, Claudio Bruno, Dariusz C Górecki
Duchenne muscular dystrophy (DMD) is the most common inherited muscle disorder that causes severe disability and death of young men. This disease is characterized by progressive muscle degeneration aggravated by sterile inflammation and is also associated with cognitive impairment and low bone density. Given that no current treatment can improve the long-term outcome, approaches with a strong translational potential are urgently needed. Duchenne muscular dystrophy (DMD) alters P2RX7 signaling in both muscle and inflammatory cells and inhibition of this receptor resulted in a significant attenuation of muscle and non-muscle symptoms in DMDmdx mouse model...
April 11, 2018: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29627451/regulation-and-function-of-avian-selenogenome
#14
REVIEW
Shuping Li, Fei Gao, Jiaqiang Huang, Yuanyuan Wu, Sen Wu, Xin Gen Lei
BACKGROUND: Selenium (Se) is an essential micronutrient required by avian species. Dietary Se/vitamin E deficiency induces three classical diseases in chicks: exudative diathesis, nutritional pancreatic atrophy, and nutritional muscular dystrophy. SCOPE OF REVIEW: This review is to summarize and analyze the evolution, regulation, and function of avian selenogenome and selenoproteome and their relationship with the three classical Se/vitamin E deficiency diseases...
April 5, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29625557/case-report-lactic-acidosis-and-rhabdomyolysis-during-telbivudine-and-tenofovir-treatment-for-chronic-hepatitis-b
#15
Yue Ying, Yue-Kai Hu, Jia-Lin Jin, Ji-Ming Zhang, Wen-Hong Zhang, Yu-Xian Huang
BACKGROUND: Current treatment options for chronic hepatitis B (CHB) are pegylated interferon alpha and nucleoside analogues (NAs). NAs have relatively fewer side effects than interferon alpha, and generally well tolerated. Previously 12.9% of patients on telbivudine treatment were reported to develop severe elevation of serum creatine phosphokinase (CPK) levels, but related clinical disease, like lactic acidosis (LA) and rhabdomyolysis (RM) were rare. The pathophysiology may be mitochondrial toxicity, for the NAs inhibit not only hepatitis B virus (HBV) polymerase, but also the host mitochondrial DNA polymerase γ...
April 6, 2018: BMC Gastroenterology
https://www.readbyqxmd.com/read/29593538/salidroside-inhibits-myogenesis-by-modulating-p-smad3-induced-myf5-transcription
#16
Peng Zhang, Wenjiong Li, Lu Wang, Hongju Liu, Jing Gong, Fei Wang, Xiaoping Chen
Aim: Salidroside is an active compound extracted from Rhodiola rosea which is used to alleviate fatigue and enhance endurance in high altitude regions. Some studies have demonstrated that salidroside can affect precursor cell differentiation in hematopoietic stem cells, erythrocytes, and osteoblasts. The aim of this study was to investigate the effect of salidroside on myoblast differentiation and to explore the underlying molecular mechanisms of this effect. Methods: C2C12 myoblast cells were treated with different concentrations of salidroside in differentiation media...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29588339/selective-prostacyclin-receptor-agonist-selexipag-in-contrast-to-prostacyclin-analogs-does-not-evoke-paradoxical-vasoconstriction-of-rat-femoral-artery
#17
Keith Morrison, Franck Haag, Roland Ernst, Marc Iglarz, Martine Clozel
Selexipag is a selective non-prostanoid prostacyclin (PGI2 ) receptor (IP receptor) agonist that is approved for the treatment of pulmonary arterial hypertension (PAH). In contrast to selexipag, PGI2 analogs used in the clinic are non-selective agonists at prostanoid receptors and can also activate contractile EP3 receptors. Leg pain is a common side effect in patients receiving treatment with PGI2 analogs and peripheral vasoconstriction can be responsible for side effects related to muscular ischemia. This study tested the hypothesis that PGI2 analogs could cause paradoxical vasoconstriction of the femoral artery via EP3 receptor activation but that only vasorelaxation would be observed in response to selexipag and its active metabolite ACT-333679...
March 27, 2018: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/29581825/novel-inhibitor-candidates-of-trpv2-prevent-damage-of-dystrophic-myocytes-and-ameliorate-against-dilated-cardiomyopathy-in-a-hamster-model
#18
Yuko Iwata, Yoshimi Katayama, Yasushi Okuno, Shigeo Wakabayashi
Transient receptor potential cation channel, subfamily V, member 2 (TRPV2) is a principal candidate for abnormal Ca2+ -entry pathways, which is a potential target for therapy of muscular dystrophy and cardiomyopathy. Here, an in silico drug screening and the following cell-based screening to measure the TRPV2 activation were carried out in HEK293 cells expressing TRPV2 using lead compounds (tranilast or SKF96365) and off-patent drug stocks. We identified 4 chemical compounds containing amino-benzoyl groups and 1 compound (lumin) containing an ethylquinolinium group as candidate TRPV2 inhibitors...
March 6, 2018: Oncotarget
https://www.readbyqxmd.com/read/29574046/editorial-commentary-preserving-myocardium-in-muscular-dystrophy-patients-using-ace-inhibition
#19
EDITORIAL
Michael D Taylor
No abstract text is available yet for this article.
February 20, 2018: Trends in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29572181/urinary-bladder-organ-hypertrophy-is-partially-regulated-by-akt1-mediated-protein-synthesis-pathway
#20
Li-Ya Qiao, Chunmei Xia, Shanwei Shen, Seong Ho Lee, Paul H Ratz, Matthew O Fraser, Amy Miner, John E Speich, Jeffrey J Lysiak, William D Steers
AIMS: The present study aims to investigate the role of Akt in the regulation of urinary bladder organ hypertrophy caused by partial bladder outlet obstruction (pBOO). MAIN METHODS: Male rats were surgically induced for pBOO. Real-time PCR and western blot were used to examine the levels of mRNA and protein. A phosphoinositide 3-kinase (PI3K) inhibitor LY294002 was used to inhibit the activity of endogenous Akt. KEY FINDINGS: The urinary bladder developed hypertrophy at 2 weeks of pBOO...
March 20, 2018: Life Sciences
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