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https://www.readbyqxmd.com/read/28089792/pharmacological-inhibition-of-pkc%C3%AE-counteracts-muscle-disease-in-a-mouse-model-of-duchenne-muscular-dystrophy
#1
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
#2
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/28077779/embryonic-exposure-to-tcdd-impacts-osteogenesis-of-the-axial-skeleton-in-japanese-medaka-oryzias-latipes
#3
AtLee T D Watson, Antonio Planchart, Carolyn J Mattingly, Christoph Winkler, David M Reif, Seth W Kullman
Recent studies from mammalian, fish, and in vitro models have identified bone and cartilage development as sensitive targets for dioxins and other aryl hydrocarbon receptor ligands. In this study, we assess how embryonic 2,3,7,8-tetrachlorochlorodibenzo-p-dioxin (TCDD) exposure impacts axial osteogenesis in Japanese medaka (Oryzias latipes), a vertebrate model of human bone development. Embryos from inbred wild-type Orange-red Hd-dR and 3 transgenic medaka lines (twist:EGFP, osx/sp7:mCherry, col10a1:nlGFP) were exposed to 0...
November 15, 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28076930/hormone-receptor-expression-in-human-fascial-tissue
#4
C Fede, G Albertin, L Petrelli, M M Sfriso, C Biz, R De Caro, C Stecco
Many epidemiologic, clinical, and experimental findings point to sex differences in myofascial pain in view of the fact that adult women tend to have more myofascial problems with respect to men. It is possible that one of the stimuli to sensitization of fascial nociceptors could come from hormonal factors such as estrogen and relaxin, that are involved in extracellular matrix and collagen remodeling and thus contribute to functions of myofascial tissue. Immunohistochemical and molecular investigations (real-time PCR analysis) of relaxin receptor 1 (RXFP1) and estrogen receptor-alpha (ERα) localization were carried out on sample of human fascia collected from 8 volunteers patients during orthopedic surgery (all females, between 42 and 70 yrs, divided into pre- and post-menopausal groups), and in fibroblasts isolated from deep fascia, to examine both protein and RNA expression levels...
November 2, 2016: European Journal of Histochemistry: EJH
https://www.readbyqxmd.com/read/28074489/a-novel-nf-%C3%AE%C2%BAb-inhibitor-edasalonexent-cat-1004-in-development-as-a-disease-modifying-treatment-for-patients-with-duchenne-muscular-dystrophy-phase-1-safety-pharmacokinetics-and-pharmacodynamics-in-adult-subjects
#5
Joanne M Donovan, Michael Zimmer, Elliot Offman, Toni Grant, Michael Jirousek
In Duchenne muscular dystrophy (DMD), NF-κB is activated in skeletal muscle from infancy regardless of the underlying dystrophin mutation and drives inflammation and muscle degeneration while inhibiting muscle regeneration. Edasalonexent (CAT-1004) is a bifunctional orally administered small molecule that covalently links 2 compounds known to inhibit NF-κB, salicylic acid and docosahexaenoic acid (DHA). Edasalonexent is designed to inhibit activated NF-κB upon intracellular cleavage to these bioactive components...
January 11, 2017: Journal of Clinical Pharmacology
https://www.readbyqxmd.com/read/28050326/use-of-botulinum-neurotoxin-in-ophthalmology
#6
REVIEW
Emel Başar, Ceyhun Arıcı
Botulinum neurotoxin (BoNT) is the first biological toxin used in the treatment of ophthalmic diseases and to decrease skin wrinkles as an aesthetic agent. When used appropriately, it weakens the force of muscular contraction and/or inhibits glandular secretion. The most common areas for botulinum toxin treatment are the upper face, including the glabella, forehead, brows, and lateral canthal lines, or crow's feet. By relaxing the muscles causing wrinkles, non-permanent results may be achieved with its use...
December 2016: Turkish Journal of Ophthalmology
https://www.readbyqxmd.com/read/28042944/comparison-of-serum-raav-serotype-specific-antibodies-in-patients-with-duchenne-muscular-dystrophy-becker-muscular-dystrophy-inclusion-body-myositis-or-gne-myopathy
#7
Deborah Zygmunt, Kelly E Crowe, Kevin Flanigan, Paul T Martin
Recombinant Adeno-associated virus (rAAV) is a commonly used gene therapy vector for the delivery of therapeutic transgenes in a variety of human diseases, but pre-existing serum antibodies to viral capsid proteins can greatly inhibit rAAV transduction of tissues. We have assayed serum from patients with Duchenne Muscular Dystrophy (DMD), Becker Muscular Dystrophy (DMD), Inclusion Body Myositis (IBM), and GNE myopathy (GNE). These were compared to serum from otherwise normal human subjects to determine the extent of pre-existing serum antibodies to rAAVrh74, rAAV1, rAAV2, rAAV6, rAAV8 and rAAV9...
January 2, 2017: Human Gene Therapy
https://www.readbyqxmd.com/read/28035339/emerging-roles-for-histone-deacetylases-in-age-related-muscle-atrophy
#8
REVIEW
Michael E Walsh, Holly Van Remmen
BACKGROUND: Skeletal muscle atrophy during aging, a process known as sarcopenia, is associated with muscle weakness, frailty, and the loss of independence in older adults. The mechanisms contributing to sarcopenia are not totally understood, but muscle fiber loss due to apoptosis, reduced stimulation of anabolic pathways, activation of catabolic pathways, denervation, and altered metabolism have been observed in muscle from old rodents and humans. OBJECTIVE: Recently, histone deacetylases (HDACs) have been implicated in muscle atrophy and dysfunction due to denervation, muscular dystrophy, and disuse, and HDACs play key roles in regulating metabolism in skeletal muscle...
October 27, 2016: Nutr Healthy Aging
https://www.readbyqxmd.com/read/28002607/targeting-of-mir-432-to-myozenin1-to-regulate-myoblast-proliferation-and-differentiation
#9
R M Ren, H Liu, S H Zhao, J H Cao
MicroRNAs (miRNAs) play important roles in the development and biochemical functions of skeletal muscles. However, targeting of miRNAs to structural genes involved in Z-discs have not been investigated. Here, we describe a highly expressed miRNA, miR-432, in pig embryonic skeletal muscle, which appeared to target myozenin1 (MYOZ1), a protein involved in the muscular sarcomere microstructure. Our results showed that miR-432 is involved in muscle development in the developing pig. In addition, it promoted differentiation of the C2C12 myoblast cell line into myotubes...
December 19, 2016: Genetics and Molecular Research: GMR
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
#10
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/27926859/rapamycin-reverses-metabolic-deficits-in-lamin-a-c-deficient-mice
#11
Chen-Yu Liao, Sydney S Anderson, Nicole H Chicoine, Jarrott R Mayfield, Emmeline C Academia, Joy A Wilson, Chalermkwan Pongkietisak, Morgan A Thompson, Earl P Lagmay, Delana M Miller, Yueh-Mei Hsu, Mark A McCormick, Monique N O'Leary, Brian K Kennedy
The role of the mTOR inhibitor, rapamycin, in regulation of adiposity remains controversial. Here, we evaluate mTOR signaling in lipid metabolism in adipose tissues of Lmna(-/-) mice, a mouse model for dilated cardiomyopathy and muscular dystrophy. Lifespan extension by rapamycin is associated with increased body weight and fat content, two phenotypes we link to suppression of elevated energy expenditure. In both white and brown adipose tissue of Lmna(-/-) mice, we find that rapamycin inhibits mTORC1 but not mTORC2, leading to suppression of elevated lipolysis and restoration of thermogenic protein UCP1 levels, respectively...
December 6, 2016: Cell Reports
https://www.readbyqxmd.com/read/27911406/ultrasound-guided-botulinum-toxin-a-injections-a-method-of-treating-sialorrhea
#12
Pierangelo Barbero, Marco Busso, Carlo Alberto Artusi, Stefania De Mercanti, Marco Tinivella, Andrea Veltri, Luca Durelli, Marinella Clerico
Neurological diseases can be complicated by sialorrhea, an excessive flow of saliva. Patients suffering from moderate to severe sialorrhea have an impaired quality of life, often worsened by correlated complications such as aspiration pneumonia, oral infections, dental caries, and maceration of the skin. Diverse therapeutic approaches have been proposed for the treatment of sialorrhea, including surgery and the use of anticholinergic agents, with limited results and the possible occurrence of serious adverse events...
November 9, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/27911334/matrix-metalloproteinases-and-tissue-inhibitor-of-metalloproteinases-in%C3%A2-inflammation-and-fibrosis-of-skeletal-muscles
#13
Hala S Alameddine, Jennifer E Morgan
In skeletal muscles, levels and activity of Matrix MetalloProteinases (MMPs) and Tissue Inhibitors of MetalloProteinases (TIMPs) have been involved in myoblast migration, fusion and various physiological and pathological remodeling situations including neuromuscular diseases. This has opened perspectives for the use of MMPs' overexpression to improve the efficiency of cell therapy in muscular dystrophies and resolve fibrosis. Alternatively, inhibition of individual MMPs in animal models of muscular dystrophies has provided evidence of beneficial, dual or adverse effects on muscle morphology or function...
November 29, 2016: Journal of Neuromuscular Diseases
https://www.readbyqxmd.com/read/27906078/four-week-rapamycin-treatment-improves-muscular-dystrophy-in-a-fukutin-deficient-mouse-model-of-dystroglycanopathy
#14
Steven J Foltz, Junna Luan, Jarrod A Call, Ankit Patel, Kristen B Peissig, Marisa J Fortunato, Aaron M Beedle
BACKGROUND: Secondary dystroglycanopathies are a subset of muscular dystrophy caused by abnormal glycosylation of α-dystroglycan (αDG). Loss of αDG functional glycosylation prevents it from binding to laminin and other extracellular matrix receptors, causing muscular dystrophy. Mutations in a number of genes, including FKTN (fukutin), disrupt αDG glycosylation. METHODS: We analyzed conditional Fktn knockout (Fktn KO) muscle for levels of mTOR signaling pathway proteins by Western blot...
June 2, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906065/dystrophin-deficient-dogs-with-reduced-myostatin-have-unequal-muscle-growth-and-greater-joint-contractures
#15
Joe N Kornegay, Daniel J Bogan, Janet R Bogan, Jennifer L Dow, Jiahui Wang, Zheng Fan, Naili Liu, Leigh C Warsing, Robert W Grange, Mihye Ahn, Cynthia J Balog-Alvarez, Steven W Cotten, Monte S Willis, Candice Brinkmeyer-Langford, Hongtu Zhu, Joe Palandra, Carl A Morris, Martin A Styner, Kathryn R Wagner
BACKGROUND: Myostatin (Mstn) is a negative regulator of muscle growth whose inhibition promotes muscle growth and regeneration. Dystrophin-deficient mdx mice in which myostatin is knocked out or inhibited postnatally have a less severe phenotype with greater total mass and strength and less fibrosis and fatty replacement of muscles than mdx mice with wild-type myostatin expression. Dogs with golden retriever muscular dystrophy (GRMD) have previously been noted to have increased muscle mass and reduced fibrosis after systemic postnatal myostatin inhibition...
April 4, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27904496/adipose-derived-stem-cells-enhance-myogenic-differentiation-in-the-mdx-mouse-model-of-muscular-dystrophy-via-paracrine-signaling
#16
Ji-Qing Cao, Ying-Yin Liang, Ya-Qin Li, Hui-Li Zhang, Yu-Ling Zhu, Jia Geng, Li-Qing Yang, Shan-Wei Feng, Juan Yang, Jie Kong, Cheng Zhang
Adipose-derived stem cells have been shown to promote peripheral nerve regeneration through the paracrine secretion of neurotrophic factors. However, it is unclear whether these cells can promote myogenic differentiation in muscular dystrophy. Adipose-derived stem cells (6 × 10(6)) were injected into the gastrocnemius muscle of mdx mice at various sites. Dystrophin expression was found in the muscle fibers. Phosphorylation levels of Akt, mammalian target of rapamycin (mTOR), eIF-4E binding protein 1 and S6 kinase 1 were increased, and the Akt/mTOR pathway was activated...
October 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27882347/ml372-blocks-smn-ubiquitination-and-improves-spinal-muscular-atrophy-pathology-in-mice
#17
Mahlet B Abera, Jingbo Xiao, Jonathan Nofziger, Steve Titus, Noel Southall, Wei Zheng, Kasey E Moritz, Marc Ferrer, Jonathan J Cherry, Elliot J Androphy, Amy Wang, Xin Xu, Christopher Austin, Kenneth H Fischbeck, Juan J Marugan, Barrington G Burnett
Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease and one of the leading inherited causes of infant mortality. SMA results from insufficient levels of the survival motor neuron (SMN) protein, and studies in animal models of the disease have shown that increasing SMN protein levels ameliorates the disease phenotype. Our group previously identified and optimized a new series of small molecules, with good potency and toxicity profiles and reasonable pharmacokinetics, that were able to increase SMN protein levels in SMA patient-derived cells...
November 17, 2016: JCI Insight
https://www.readbyqxmd.com/read/27881412/renin-angiotensin-aldosterone-system-inhibitors-improve-membrane-stability-and-change-gene-expression-profiles-in-dystrophic-skeletal-muscles
#18
Jessica A Chadwick, Sayak Bhattacharya, Jeovanna Lowe, Noah Weisleder, Jill A Rafael-Fortney
Angiotensin-converting enzyme inhibitors and mineralocorticoid receptor (MR) antagonists are FDA approved drugs that inhibit the renin-angiotensin-aldosterone system (RAAS) and are used to treat heart failure. Combined treatment with the angiotensin-converting enzyme inhibitor lisinopril and the non-specific MR antagonist spironolactone surprisingly improves skeletal muscle, in addition to heart function and pathology in a Duchenne muscular dystrophy mouse model. We recently demonstrated that MR is present in all limb and respiratory muscles and functions as a steroid hormone receptor in differentiated normal human skeletal muscle fibers...
November 23, 2016: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/27874066/cl316-243-a-%C3%AE-3-adrenergic-receptor-agonist-induces-muscle-hypertrophy-and-increased-strength
#19
Daniela Puzzo, Roberto Raiteri, Clotilde Castaldo, Raffaele Capasso, Ester Pagano, Mariateresa Tedesco, Walter Gulisano, Lisaveta Drozd, Pellegrino Lippiello, Agostino Palmeri, Pietro Scotto, Maria Concetta Miniaci
Studies in vitro have demonstrated that β3-adrenergic receptors (β3-ARs) regulate protein metabolism in skeletal muscle by promoting protein synthesis and inhibiting protein degradation. In this study, we evaluated whether activation of β3-ARs by the selective agonist CL316,243 modifies the functional and structural properties of skeletal muscles of healthy mice. Daily injections of CL316,243 for 15 days resulted in a significant improvement in muscle force production, assessed by grip strength and weight tests, and an increased myofiber cross-sectional area, indicative of muscle hypertrophy...
November 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27873355/isoquercitrin-protects-against-pulmonary-hypertension-via-inhibiting-pasmcs-proliferation
#20
Yongtao Zhang, Yuqian Cui, Wei Deng, Hao Wang, Weidong Qin, Chengmin Huang, Chen Li, Jianning Zhang, Yuan Guo, Dawei Wu, Haipeng Guo
Pulmonary vascular remodeling is a common feature among the heterogeneous disorders that cause pulmonary arterial hypertension (PAH), and pulmonary arterial smooth muscle cells (PASMCs) proliferation impact the long-term prognosis of the patient. Isoquercitrin (IQC) is a flavonoid with anti-oxidative, anti-inflammatory and anti-proliferative activations. This study aimed to investigate whether IQC could prevent PASMCs proliferation and vascular remodeling in monocrotaline (MCT) induced PAH. Male Wistar rats were administered with vehicle or 0...
November 22, 2016: Clinical and Experimental Pharmacology & Physiology
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