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https://www.readbyqxmd.com/read/28108217/cdk3-is-a-major-target-of-mir-150-in-cell-proliferation-and-anti-cancer-effect
#1
Liang Wang, Yongyong Xi, Chengcao Sun, Feng Zhang, Heng Jiang, Qiqiang He, Dejia Li
MiR-150, a member of small non-coding RNAs, has been proven to dysregulate in different types of tumor and bear on carcinogenesis and cancer prognosis by regulating the expression of a series of gene including utrophin. Given that utrophin can compensate for dystrophin's absence and be regarded as a promising therapeutic target for Duchenne Muscular Dystrophy (DMD), we further detected the deep role of miR-150 in dystrophic muscle. Using a range of bioinformatic, molecular and cell biology techniques, we declared that miR-150 directly targets cyclin-dependent kinase 3 (CDK3) and leads to the regulation of CDK3 gene expression in both muscle-derived and non-muscle cells...
January 17, 2017: Experimental and Molecular Pathology
https://www.readbyqxmd.com/read/28103859/treatment-with-soluble-activin-type-iib-receptor-improves-bone-mass-and-strength-in-a-mouse-model-of-duchenne-muscular-dystrophy
#2
Tero Puolakkainen, Hongqian Ma, Heikki Kainulainen, Arja Pasternack, Timo Rantalainen, Olli Ritvos, Kristiina Heikinheimo, Juha J Hulmi, Riku Kiviranta
BACKGROUND: Inhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength. Duchenne muscular dystrophy (DMD) is a neuromuscular disorder that leads to progressive muscle degeneration and also high incidence of fractures. The aim of our study was to test whether inhibition of activin receptor IIB ligands with or without exercise could improve bone strength in the mdx mouse model for DMD. METHODS: Thirty-two mdx mice were divided to running and non-running groups and to receive either PBS control or soluble activin type IIB-receptor (ActRIIB-Fc) once weekly for 7 weeks...
January 19, 2017: BMC Musculoskeletal Disorders
https://www.readbyqxmd.com/read/28089792/pharmacological-inhibition-of-pkc%C3%AE-counteracts-muscle-disease-in-a-mouse-model-of-duchenne-muscular-dystrophy
#3
V Marrocco, P Fiore, A Benedetti, S Pisu, E Rizzuto, A Musarò, L Madaro, B Lozanoska-Ochser, M Bouché
: Inflammation plays a considerable role in the progression of Duchenne Muscular Dystrophy (DMD), a severe muscle disease caused by a mutation in the dystrophin gene. We previously showed that genetic ablation of Protein Kinase C θ (PKCθ) in mdx, the mouse model of DMD, improves muscle healing and regeneration, preventing massive inflammation. To establish whether pharmacological targeting of PKCθ in DMD can be proposed as a therapeutic option, in this study we treated young mdx mice with the PKCθ inhibitor Compound 20 (C20)...
January 7, 2017: EBioMedicine
https://www.readbyqxmd.com/read/28087735/relationships-linking-emotional-motor-cognitive-and-gabaergic-dysfunctions-in-dystrophin-deficient-mdx-mice
#4
Cyrille Vaillend, Rémi Chaussenot
Alterations in the Duchenne muscular dystrophy (DMD) gene have been associated with enhanced stress reactivity in vertebrate species, suggesting a role for brain dystrophin in fear-related behavioral and cognitive processes. Because the loss of dystrophin (Dp427) reduces clustering of central GABAA receptors, it is suspected that local inhibitory tuning and modulation of neuronal excitability are perturbed in a distributed brain circuit that normally controls such critical behavioral functions. In this study we undertook a large-scale behavioral study to evaluate fear-related behavioral disturbances in dystrophin-deficient mdx mice...
January 13, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28063157/a-new-method-of-genotyping-mdx-4cv-mice-by-pcr-rflp-analysis
#5
Elisia D Tichy, Foteini Mourkioti
INTRODUCTION: The mdx(4cv) mouse is a common model to study Duchenne muscular dystrophy (DMD). The most utilized methodology to identify the genotype of these mice is Sanger DNA sequencing. METHODS: Here, we provide a simple, cost-effective alternative approach to identify the wildtype, heterozygous, or homozygous/hemizygous genotypes of these mice, using commonly available laboratory equipment and reagents. RESULTS: Our technique exploits a restriction fragment length polymorphism (RFLP) that is generated by the point mutation found in exon 53 of mdx(4cv) mice...
January 7, 2017: Muscle & Nerve
https://www.readbyqxmd.com/read/28057817/contractile-efficiency-of-dystrophic-mdx-mouse-muscle-in-vivo-and-ex-vivo-assessment-of-adaptation-to-exercise-of-functional-end-points
#6
Roberta Francesca Capogrosso, Paola Mantuano, Anna Cozzoli, Francesca Sanarica, Ada Maria Massari, Elena Conte, Adriano Fonzino, Arcangela Giustino, Jean-Francois Rolland, Angelo Quaranta, Michela De Bellis, Giulia Maria Camerino, Robert W Grange, Annamaria De Luca
Progressive weakness is a typical feature of Duchenne muscular dystrophy (DMD) patients and is exacerbated in the benign mdx mouse model by in vivo treadmill exercise. We hypothesized a different threshold for functional adaptation of mdx muscles in response to the duration of the exercise protocol. In vivo weakness was confirmed by grip strength after 4, 8 and 12 weeks of exercise in mdx mice. Torque measurements revealed that exercise-related weakness in mdx mice correlated with the duration of the protocol, while wild-type (wt) mice were stronger...
January 5, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28056487/non-invasive-assessment-of-muscle-injury-in-healthy-and-dystrophic-animals-with-electrical-impedance-myography
#7
Benjamin Sanchez, Shama R Iyer, Jia Li, Kush Kapur, Su Xu, Seward Rutkove, Richard M Lovering
INTRODUCTION: Dystrophic muscle is particularly susceptible to eccentric contraction-induced injury. We tested the hypothesis that electrical impedance myography (EIM) can detect injury induced by maximal-force lengthening contractions. METHODS: We induced injury in the quadriceps of wild type (WT) and dystrophic (mdx) mice with eccentric contractions using an established model. RESULTS: mdx quadriceps had significantly larger losses in peak twitch and tetany compared to losses in WT quadriceps...
January 5, 2017: Muscle & Nerve
https://www.readbyqxmd.com/read/28043590/use-of-wgs-in-mycobacterium-tuberculosis-routine-diagnosis
#8
Daniela M Cirillo, Andrea M Cabibbe, Maria Rosaria De Filippo, Alberto Trovato, Tullia Simonetti, Gian Maria Rossolini, Enrico Tortoli
OBJECTIVE/BACKGROUND: Whole Genome Sequencing (WGS) is becoming affordable with overall costs comparable to other tests currently in use to perform the diagnosis of drug-resistant tuberculosis (TB) and cluster analysis. The WGS approach allows an "all-in-one" approach providing results on expected sensitivity of the strains, genetic background, epidemiological data, and indication of risk of laboratory cross-contamination. METHODS: Although ideal, WGS from the direct diagnostic specimen is not yet standardized, and to date the two most promising approaches are WGS from early positive liquid culture and targeted sequencing from diagnostic specimens using Next-Generation Technology...
December 2016: International Journal of Mycobacteriology
https://www.readbyqxmd.com/read/28041995/osteoprotegerin-and-%C3%AE-2-agonists-mitigate-muscular-dystrophy-in-slow-and-fast-twitch-skeletal-muscles
#9
Sébastien S Dufresne, Antoine Boulanger-Piette, Jérôme Frenette
Our recent work showed that daily injections of osteoprotegerin (OPG)-immunoglobulin fragment complex (OPG-Fc) completely restore the function of fast-twitch extensor digitorum longus muscles in dystrophic mdx mice, a murine model of Duchenne muscular dystrophy. However, despite marked improvements, OPG-Fc was not as effective in preventing the loss of function of slow-twitch soleus and diaphragm muscles. Because β2-agonists enhance the function of slow- and fast-twitch dystrophic muscles and because their use is limited by their adverse effects on bone and cardiac tissues, we hypothesized that OPG-Fc, a bone and skeletal muscle protector, acts synergistically with β2-agonists and potentiates their positive effects on skeletal muscles...
December 30, 2016: American Journal of Pathology
https://www.readbyqxmd.com/read/28028563/whole-genome-sequencing-reveals-a-7-base-pair-deletion-in-dmd-exon-42-in-a-dog-with-muscular-dystrophy
#10
Peter P Nghiem, Luca Bello, Cindy Balog-Alvarez, Sara Mata López, Amanda Bettis, Heather Barnett, Briana Hernandez, Scott J Schatzberg, Richard J Piercy, Joe N Kornegay
Dystrophin is a key cytoskeletal protein coded by the Duchenne muscular dystrophy (DMD) gene located on the X-chromosome. Truncating mutations in the DMD gene cause loss of dystrophin and the classical DMD clinical syndrome. Spontaneous DMD gene mutations and associated phenotypes occur in several other species. The mdx mouse model and the golden retriever muscular dystrophy (GRMD) canine model have been used extensively to study DMD disease pathogenesis and show efficacy and side effects of putative treatments...
December 27, 2016: Mammalian Genome: Official Journal of the International Mammalian Genome Society
https://www.readbyqxmd.com/read/28018975/disease-modifying-effects-of-orally-bioavailable-nf-%C3%AE%C2%BAb-inhibitors-in-dystrophin-deficient-muscle
#11
David W Hammers, Margaret M Sleeper, Sean C Forbes, Cora C Coker, Michael R Jirousek, Michael Zimmer, Glenn A Walter, H Lee Sweeney
Duchenne muscular dystrophy (DMD) is a devastating muscle disease characterized by progressive muscle deterioration and replacement with an aberrant fatty, fibrous matrix. Chronic upregulation of nuclear factor κB (NF-κB) is implicated as a driver of the dystrophic pathogenesis. Herein, 2 members of a novel class of NF-κB inhibitors, edasalonexent (formerly CAT-1004) and CAT-1041, were evaluated in both mdx mouse and golden retriever muscular dystrophy (GRMD) dog models of DMD. These orally bioavailable compounds consist of a polyunsaturated fatty acid conjugated to salicylic acid and potently suppress the pathogenic NF-κB subunit p65/RelA in vitro...
December 22, 2016: JCI Insight
https://www.readbyqxmd.com/read/28004656/co-delivery-of-indoleamine-2-3-dioxygenase-prevents-loss-of-expression-of-an-antigenic-transgene-in-dystrophic-mouse-muscles
#12
D Sharma, R Al-Khalidi, S Edgar, Q An, Y Wang, C Young, D Nowis, D C Gorecki
A significant problem affecting gene therapy approaches aiming at achieving long-term transgene expression is the immune response against the protein product of the therapeutic gene, which can reduce or eliminate the therapeutic effect. The problem is further exacerbated when therapy involves targeting an immunogenic tissue and/or one with a pre-existing inflammatory phenotype, such as dystrophic muscles. In this proof-of-principle study, we co-expressed a model antigen, bacterial β-galactosidase, with an immunosuppressive factor, indoleamine 2,3-dioxygenase 1 (IDO1), in muscles of the mdx mouse model of Duchenne muscular dystrophy...
December 22, 2016: Gene Therapy
https://www.readbyqxmd.com/read/28003225/muscles-specific-microrna-206-targets-multiple-components-in-dystrophic-skeletal-muscle-representing-beneficial-adaptations
#13
Adel Amirouche, Vanessa E Jahnke, John A Lunde, Nathalie Koulmann, Damien G Freyssenet, Bernard J Jasmin
Over the last several years, converging lines of evidence have indicated that miR-206 plays a pivotal role in promoting muscle differentiation and regeneration, thereby potentially impacting positively on the progression of neuromuscular disorders including Duchenne muscular dystrophy (DMD). Despite several studies showing the regulatory function of miR-206 on target mRNAs in skeletal muscle cells, the effects of overexpression of miR-206 in dystrophic muscles remain to be established. Here, we found that miR-206 overexpression in mdx mouse muscles simultaneously targets multiple mRNAs and proteins implicated in satellite cell differentiation, muscle regeneration, and at the neuromuscular junction...
December 21, 2016: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/27997693/genetic-ablation-of-p65-subunit-of-nf-%C3%AE%C2%BAb-in-mdx-mice-to-improve-muscle-physiological-function
#14
Xi Yin, Ying Tang, Jian Li, Anna T Dzuricky, Chuanqiang Pu, Freddie Fu, Bing Wang
INTRODUCTION: Duchenne muscular dystrophy (DMD) is a genetic muscle disease characterized by dystrophin deficiency. Beyond gene replacement, the question of whether ablation of the p65 gene of nuclear factor-kappa B (NF-κB) in DMD can improve muscle physiology function is unknown. In this study, we investigated muscle physiological improvement in mdx mice (DMD model) with a genetic reduction of NF-κB. METHODS: Muscle physiological function and histology were studied in 2-month-old mdx/p65(+/-) , wild-type (WT), mdx, and human minidystrophin gene transgenic mdx (TghΔDys/mdx) mice...
December 20, 2016: Muscle & Nerve
https://www.readbyqxmd.com/read/27988307/interleukin-6-and-neuregulin-1-as-regulators-of-utrophin-expression-via-the-activation-of-nrg-1-erbb-signaling-pathway-in-mdx-cells
#15
Nevenka Juretić, Josefina Díaz, Felipe Romero, Gustavo González, Enrique Jaimovich, Nora Riveros
Duchenne muscular dystrophy (DMD) is a neuromuscular disease originated by mutations in the dystrophin gene. A promising therapeutic approach deals with functional substitution of dystrophin by utrophin, a structural homolog that might be able to compensate dystrophin absence in DMD muscle fibers. It has been described that both interleukin-6 (IL-6) and neuregulin-1 (NRG-1; Heregulin-HRG) induce utrophin expression in skeletal muscle. We investigated a possible functional link among IL-6, NRG-1 and utrophin, in normal (C57) and dystrophic (mdx) skeletal muscle cells...
December 15, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27979987/altered-nuclear-dynamics-in-mdx-myofibers
#16
Shama R Iyer, Sameer B Shah, Ana P Valencia, Martin F Schneider, Erick O Hernandez-Ochoa, Joseph P Stains, Silvia S Blemker, Richard M Lovering
Duchenne muscular dystrophy (DMD) is a genetic disorder in which the absence of dystrophin leads to progressive muscle degeneration and weakness. While the genetic basis is known, the pathophysiology of dystrophic skeletal muscle remains unclear. We examined nuclear movement in wild type (WT) and dystrophin-null (MDX) mouse myofibers. We also examined expression of proteins in the LINC (linkers of nucleoskeleton and cytoskeleton) complex as well as nuclear transcriptional activity via histone H3 acetylation and polyadenylate-binding nuclear protein-1...
December 15, 2016: Journal of Applied Physiology
https://www.readbyqxmd.com/read/27975174/dysregulation-of-intracellular-ca-2-in-dystrophic-cortical-and-hippocampal-neurons
#17
José R Lopez, Juan Kolster, Arkady Uryash, Eric Estève, Francisco Altamirano, José A Adams
Duchenne muscular dystrophy (DMD) is an inherited X-linked disorder characterized by skeletal muscle wasting, cardiomyopathy, as well as cognitive impairment. Lack of dystrophin in striated muscle produces dyshomeostasis of resting intracellular Ca(2+) ([Ca(2+)]i), Na(+) ([Na(+)]i), and oxidative stress. Here, we test the hypothesis that similar to striated muscle cells, an absence of dystrophin in neurons from mdx mice (a mouse model for DMD) is also associated with dysfunction of [Ca(2+)]i homeostasis and oxidative stress...
December 15, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27956144/self-aggregating-1-8kda-polyethylenimines-with-dissolution-switch-at-endosomal-acidic-ph-are-delivery-carriers-for-plasmid-dna-mrna-sirna-and-exon-skipping-oligonucleotides
#18
Manuela Chiper, Nassera Tounsi, Ryszard Kole, Antoine Kichler, Guy Zuber
Efficiency of polyethylenimine (PEI) for nucleic acid delivery is affected by the size of the carrier and length of the nucleic acids. For instance, PEIs with molecular weights between 10-30kDa provide optimal DNA delivery activity whereas PEIs with molecular weights below 1.8kDa are ineffective. The activity of PEI is also severely diminished by substitution of DNA for shorter nucleic acids such as mRNA or siRNA. Here, through chemical modification of the primary amines to aromatic domains we achieved nucleic acid delivery by the 1...
December 9, 2016: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/27932677/suite-of-clinically-relevant-functional-assays-to-address-therapeutic-efficacy-and-disease-mechanism-in-the-dystrophic-mdx-mouse
#19
Yafeng Song, Shira Tziporah Rosenblum, Leon Morales, Mihail Petrov, Christopher Greer, Samantha Globerman, Hansell H Stedman
Duchenne muscular dystrophy (DMD) is a progressive primary myodegenerative disease caused by a genetic deficiency of the 427 KD cytoskeletal protein dystrophin. Despite its single-gene etiology, DMD's complex pathogenesis remains poorly understood, complicating the extrapolation from results of preclinical studies in genetic homologues to the design of informative clinical trials. Here we describe novel phenotypic assays which when applied to the mdx mouse resemble recently used primary endpoints for DMD clinical trials...
December 8, 2016: Journal of Applied Physiology
https://www.readbyqxmd.com/read/27931510/generation-of-equine-induced-pluripotent-stem-cells-and-analysis-of-their-therapeutic-potential-for-muscle-injuries
#20
Eun-Mi Lee, Ah-Young Kim, Eun-Joo Lee, Jin-Kyu Park, Se-Il Park, Ssang-Goo Cho, Hong Kyun Kim, Shin-Yoon Kim, Kyu-Shik Jeong
Horse health has become a major concern with the expansion of horse-related industries and sports; the importance of healthy muscles for horse performance and daily activities is undisputed. Here we generated equine-induced pluripotent stem cells (E-iPSCs) by reprogramming equine adipose-derived stem cells (E-ADSCs) into iPSCs using a polycistronic lentiviral vector encoding four transcription factors (i.e., Oct4, Sox2, Klf4, and c-Myc) and then examined their pluripotent characteristics. Subsequently, established E-iPSCs were transplanted into muscle-injured Rag/mdx mice...
November 2016: Cell Transplantation
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