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sln, mice, mdxutr, muscle, pubmed, article, google, scholar, expression, fig, cas, muscles, dmd, skeletal, function, serca, muscular, dystrophy, tko, cardiac, significantly, data, dystrophic, diaphragm, increased, aav, protein, findings, levels, reduction, central, supplementary, duchenne, nature, uptake, gene, shown, mouse, quadriceps, force, cardiomyopathy, tissues, reduced, dogs, correction, cell, sarcolipin, welchs, size, treatment,

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nature portfolio itr-u6-promoter-shsln-bghpa-itr resulting plasmid “pfb-itr-sh-sln” recombinant baculovirus “bac-itr-sh-sln” privacy policy eu/research/preclinical/dmd-sops/ calpain substrate ac-lly-afc advertising biomedical research bridge-grant semi-quantitative rt-pcr data progressive nature muscle development social media ad libitum access nature 360 nature 484 nature reprints thermofisher scientific targeting sln expression/function bac-itr-sh-sln endogenous full-length utrophin endoplasmic reticulum–mitochondria crosstalk dystrophin/utrophin double mutant animal research kaplan–meier survival analysis nebulin-free skeletal muscle sarcoplasmic reticulum ca-atpase kaplan–meier survival curves force-frequency curves indicating small stripes based author information authors fast-twitch skeletal muscles32 mitigates skeletal muscle x-linked disease caused 9-mediated rna interference prevents fiber-type transition allergen-sensitized mouse model duchenne muscular dystrophy permissions decreased sarco/endoplasmic reticulum post-hoc bonferroni correction nonparametric log-rank test research prevent fiber-type transition sr ca2+ content excitation-contraction coupling proteins exacerbated muscle atrophy markedly abnormal mitochondria diet induced diabetes

Questions {❓}

• Is the fundamental pathology in Duchenne's muscular dystrophy caused by a failure of glycogenolysis–glycolysis in costameres?

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         description:Sarcolipin (SLN) is an inhibitor of the sarco/endoplasmic reticulum (SR) Ca2+ 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. To translate our findings into a therapeutic strategy, we knock down SLN expression in 1-month old mdx:utr −/− mice via adeno-associated virus (AAV) 9-mediated RNA interference. The AAV treatment markedly reduces SLN expression, attenuates muscle pathology and improves diaphragm, skeletal muscle and cardiac function. Taken together, our findings suggest that SLN reduction is a promising therapeutic approach for DMD. Sarcolipin is an inhibitor of the ATP dependent calcium pump SERCA, and is abnormally elevated in Duchenne muscular dystrophy. The authors show that reducing sarcolipin expression ameliorates skeletal muscle pathology and cardiomyopathy and extends life span in mouse models of DMD.
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PostalAddress:
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Department of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, USA
      name:Department of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Department of Medicine, University of Alabama at Birmingham, and Birmingham VA Medical Center, Birmingham, USA
      name:Department of Pediatrics and Department of Neurology, Ohio State University Research Institute at Nationwide Children’s Hospital, Columbus, USA
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, USA
      name:Department of Molecular Microbiology and Immunology, Neurology, Bioengineering, Biomedical Sciences, The University of Missouri, Columbia, USA
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA
      name:Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, USA

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