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63. The muscular dystrophies: from genes to therapies

Author

Lovering, Richard M., Porter, Neil C., and Bloch, Robert J.

Subjects
Muscular dystrophy -- Genetic aspects -- Care and treatment, Health
Abstract

The genetic basis of many muscular disorders, including many of the more common muscular dystrophies, is now known. Clinically, the recent genetic advances have improved diagnostic capabilities, but they have not yet provided clues about treatment or management. Thanks to better management strategies and therapeutic interventions, however, many patients with a muscular dystrophy are more active and are living longer. Physical therapists, therefore, are more likely to see a patient with a muscular dystrophy, so understanding these muscle disorders and their management is essential. Physical therapy offers the most promise in caring for the majority of patients with these conditions, because it is unlikely that advances in gene therapy will significantly alter their clinical treatment in the near future. This perspective covers some of the basic molecular biological advances together with the clinical manifestations of the muscular dystrophies and the latest approaches to their management. Key Words: Muscular dystrophy, Skeletal muscle., The muscular dystrophies (MDs) are a heterogeneous group of inherited disorders characterized by progressive weakness and degeneration of skeletal muscles (Table). They have traditionally been classified by clinical presentation, mode [...]

Published
2005

64. DS_10.1177_0363546518769267 – Supplemental material for Fatty Infiltration Is a Prognostic Marker of Muscle Function After Rotator Cuff Tear

Author

Valencia, Ana P., Lai, Jim K., Shama R. Iyer, Mistretta, Katherine L., Spangenburg, Espen E., Davis, Derik L., Lovering, Richard M., and Mohit N. Gilotra

Subjects
FOS: Clinical medicine, 110323 Surgery, 110604 Sports Medicine, FOS: Health sciences, humanities, 110314 Orthopaedics
Abstract

Supplemental material, DS_10.1177_0363546518769267 for Fatty Infiltration Is a Prognostic Marker of Muscle Function After Rotator Cuff Tear by Ana P. Valencia, Jim K. Lai, Shama R. Iyer, Katherine L. Mistretta, Espen E. Spangenburg, Derik L. Davis, Richard M. Lovering and Mohit N. Gilotra in The American Journal of Sports Medicine

Published
2018
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65. CaMKII oxidation is a performance/disease trade-off in vertebrate evolution

Author

Wang, Qinchuan, primary, Hernández-Ochoa, Erick O., additional, Viswanathan, Meera C., additional, Blum, Ian D., additional, Granger, Jonathan M., additional, Murphy, Kevin R., additional, Wei, An-Chi, additional, Aja, Susan, additional, Liu, Naili, additional, Antonescu, Corina M., additional, Florea, Liliana D., additional, Talbot, C. Conover, additional, Mohr, David, additional, Wagner, Kathryn R., additional, Regot, Sergi, additional, Lovering, Richard M., additional, Wu, Mark N., additional, Cammarato, Anthony, additional, Schneider, Martin F., additional, Bever, Gabriel S., additional, and Anderson, Mark E., additional

Published
2019
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69. Inducedin vivoknockdown of theBrca1gene in skeletal muscle results in skeletal muscle weakness

Author

Tarpey, Michael D., primary, Valencia, Ana P., additional, Jackson, Kathryn C., additional, Amorese, Adam J., additional, Balestrieri, Nicholas P., additional, Renegar, Randall H., additional, Pratt, Stephen J. P., additional, Ryan, Terence E., additional, McClung, Joseph M., additional, Lovering, Richard M., additional, and Spangenburg, Espen E., additional

Published
2018
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71. Abnormalities in Brain and Muscle Microstructure and Neurochemistry of the DMD Rat Measured by in vivo Diffusion Tensor Imaging and High Resolution Localized 1H MRS.

Author

Xu, Su, Tang, Shiyu, Li, Xin, Iyer, Shama R., and Lovering, Richard M.

Subjects
DIFFUSION tensor imaging, HIGH resolution imaging, BRAIN abnormalities, NUCLEAR magnetic resonance spectroscopy, CENTRAL nervous system, TEMPORALIS muscle
Abstract

Duchenne muscular dystrophy (DMD) is an X-linked disorder caused by the lack of dystrophin with progressive degeneration of skeletal muscles. Most studies regarding DMD understandably focus on muscle, but dystrophin is also expressed in the central nervous system, potentially resulting in cognitive and behavioral changes. Animal models are being used for developing more comprehensive neuromonitoring protocols and clinical image acquisition procedures. The recently developed DMD rat is an animal model that parallels the progressive muscle wasting seen in DMD. Here, we studied the brain and temporalis muscle structure and neurochemistry of wild type (WT) and dystrophic (DMD) rats using magnetic resonance imaging and spectroscopy. Both structural and neurochemistry alterations were observed in the DMD rat brain and the temporalis muscle. There was a decrease in absolute brain volume (WT = 1579 mm3; DMD = 1501 mm3; p = 0.039, Cohen's d = 1.867), but not normalized (WT = 4.27; DMD = 4.02; p = 0.306) brain volume. Diffusion tensor imaging (DTI) revealed structural alterations in the DMD temporalis muscle, with increased mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD). In the DMD rat thalamus, DTI revealed an increase in fractional anisotropy (FA) and a decrease in RD. Smaller normalized brain volume correlated to severity of muscle dystrophy (r = −0.975). Neurochemical changes in the DMD rat brain included increased GABA and NAA in the prefrontal cortex, and GABA in the hippocampus. Such findings could indicate disturbed motor and sensory signaling, resulting in a dysfunctional GABAergic neurotransmission, and an unstable osmoregulation in the dystrophin-null brain. [ABSTRACT FROM AUTHOR]

Published
2020
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73. Induced Cre‐mediated knockdown of Brca1 in skeletal muscle reduces mitochondrial respiration and prevents glucose intolerance in adult mice on a high‐fat diet

Author

Jackson, Kathryn C., primary, Tarpey, Michael D., additional, Valencia, Ana P., additional, Iñigo, Melissa R., additional, Pratt, Stephen J., additional, Patteson, Daniel J., additional, McClung, Joseph M., additional, Lovering, Richard M., additional, Thomson, David M., additional, and Spangenburg, Espen E., additional

Published
2018
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77. Altered nuclear dynamics in MDX myofibers

Author

Iyer, Shama R., primary, Shah, Sameer B., additional, Valencia, Ana P., additional, Schneider, Martin F., additional, Hernández-Ochoa, Erick O., additional, Stains, Joseph P., additional, Blemker, Silvia S., additional, and Lovering, Richard M., additional

Published
2017
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78. NAD + repletion improves muscle function in muscular dystrophy and counters global PARylation

Author

Ryu, Dongryeol, primary, Zhang, Hongbo, additional, Ropelle, Eduardo R., additional, Sorrentino, Vincenzo, additional, Mázala, Davi A. G., additional, Mouchiroud, Laurent, additional, Marshall, Philip L., additional, Campbell, Matthew D., additional, Ali, Amir Safi, additional, Knowels, Gary M., additional, Bellemin, Stéphanie, additional, Iyer, Shama R., additional, Wang, Xu, additional, Gariani, Karim, additional, Sauve, Anthony A., additional, Cantó, Carles, additional, Conley, Kevin E., additional, Walter, Ludivine, additional, Lovering, Richard M., additional, Chin, Eva R., additional, Jasmin, Bernard J., additional, Marcinek, David J., additional, Menzies, Keir J., additional, and Auwerx, Johan, additional

Published
2016
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79. Induced in vivo knockdown of the Brca1 gene in skeletal muscle results in skeletal muscle weakness.

Author

Tarpey, Michael D., Valencia, Ana P., Jackson, Kathryn C., Amorese, Adam J., Balestrieri, Nicholas P., Renegar, Randall H., Pratt, Stephen J. P., Ryan, Terence E., McClung, Joseph M., Lovering, Richard M., and Spangenburg, Espen E.

Subjects
SKELETAL muscle, BRCA genes, MUSCLE weakness, DNA ligases, RESPIRATORY muscles, DNA repair
Abstract

Key points: Breast cancer 1 early onset gene codes for the DNA repair enzyme, breast cancer type 1 susceptibility protein (BRCA1). The gene is prone to mutations that cause a loss of protein function.BRCA1/Brca1 has recently been found to regulate several cellular pathways beyond DNA repair and is expressed in skeletal muscle.Skeletal muscle specific knockout of Brca1 in mice caused a loss of muscle quality, identifiable by reductions in muscle force production and mitochondrial respiratory capacity.Loss of muscle quality was associated with a shift in muscle phenotype and an accumulation of mitochondrial DNA mutations.These results demonstrate that BRCA1 is necessary for skeletal muscle function and that increased mitochondrial DNA mutations may represent a potential underlying mechanism. Recent evidence suggests that the breast cancer 1 early onset gene (BRCA1) influences numerous peripheral tissues, including skeletal muscle. The present study aimed to determine whether induced‐loss of the breast cancer type 1 susceptibility protein (Brca1) alters skeletal muscle function. We induced genetic ablation of exon 11 in the Brca1 gene specifically in the skeletal muscle of adult mice to generate skeletal muscle‐specific Brca1 homozygote knockout (Brca1KOsmi) mice. Brca1KOsmi exhibited kyphosis and decreased maximal isometric force in limb muscles compared to age‐matched wild‐type mice. Brca1KOsmi skeletal muscle shifted toward an oxidative muscle fibre type and, in parallel, increased myofibre size and reduced capillary numbers. Unexpectedly, myofibre bundle mitochondrial respiration was reduced, whereas contraction‐induced lactate production was elevated in Brca1KOsmi muscle. Brca1KOsmi mice accumulated mitochondrial DNA mutations and exhibited an altered mitochondrial morphology characterized by distorted and enlarged mitochondria, and these were more susceptible to swelling. In summary, skeletal muscle‐specific loss of Brca1 leads to a myopathy and mitochondriopathy characterized by reductions in skeletal muscle quality and a consequent kyphosis. Given the substantial impact of BRCA1 mutations on cancer development risk in humans, a parallel loss of BRCA1 function in patient skeletal muscle cells would potentially result in implications for human health. Key points: Breast cancer 1 early onset gene codes for the DNA repair enzyme, breast cancer type 1 susceptibility protein (BRCA1). The gene is prone to mutations that cause a loss of protein function.BRCA1/Brca1 has recently been found to regulate several cellular pathways beyond DNA repair and is expressed in skeletal muscle.Skeletal muscle specific knockout of Brca1 in mice caused a loss of muscle quality, identifiable by reductions in muscle force production and mitochondrial respiratory capacity.Loss of muscle quality was associated with a shift in muscle phenotype and an accumulation of mitochondrial DNA mutations.These results demonstrate that BRCA1 is necessary for skeletal muscle function and that increased mitochondrial DNA mutations may represent a potential underlying mechanism. [ABSTRACT FROM AUTHOR]

Published
2019
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85. Effects of in vivo injury on the neuromuscular junction in healthy and dystrophic muscles

Author

Pratt, Stephen JP, Shah, Sameer B, Ward, Christopher W, Inacio, Mario P, Stains, Joseph P, and Lovering, Richard M

Subjects
Neuromuscular Junction, Gene Expression, Receptor Protein-Tyrosine Kinases, musculoskeletal system, Bungarotoxins, Motor Endplate, Axons, Dystrophin, Mice, Inbred C57BL, Muscular Dystrophy, Duchenne, Mice, Torque, Isometric Contraction, Animals, Receptors, Cholinergic, RNA, Messenger, Muscle, Skeletal, Skeletal Muscle and Exercise
Abstract

The most common and severe form of muscular dystrophy is Duchenne muscular dystrophy (DMD), a disorder caused by the absence of dystrophin, a structural protein found on the cytoplasmic surface of the sarcolemma of striated muscle fibres. Considerable attention has been dedicated to studying myofibre damage and muscle plasticity, but there is little information to determine if damage from contraction-induced injury occurs at or near the nerve terminal axon. We used α-bungarotoxin to compare neuromuscular junction (NMJ) morphology in healthy (wild-type, WT) and dystrophic (mdx) mouse quadriceps muscles and evaluated transcript levels of the post-synaptic muscle-specific kinase signalling complex. Our focus was to study changes in NMJs after injury induced with an established in vivo animal injury model. Neuromuscular transmission, electromyography (EMG), and NMJ morphology were assessed 24 h after injury. In non-injured muscle, muscle-specific kinase expression was significantly decreased in mdx compared to WT. Injury resulted in a significant loss of maximal torque in WT (39 ± 6%) and mdx (76 ± 8%) quadriceps, but significant changes in NMJ morphology, neuromuscular transmission and EMG data were found only in mdx following injury. Compared with WT mice, motor end-plates of mdx mice demonstrated less continuous morphology, more disperse acetylcholine receptor aggregates and increased number of individual acetylcholine receptor clusters, an effect that was exacerbated following injury. Neuromuscular transmission failure increased and the EMG measures decreased after injury in mdx mice only. The data show that eccentric contraction-induced injury causes morphological and functional changes to the NMJs in mdx skeletal muscle, which may play a role in excitation-contraction coupling failure and progression of the dystrophic process.

Published
2012

86. An in vivo Rodent Model of Contraction-induced Injury and Non-invasive Monitoring of Recovery

Author

Lovering, Richard M., Roche, Joseph A., Goodall, Mariah H., Clark, Brett B., and McMillan, Alan

Subjects
Disease Models, Animal, Mice, Torque, Muscles, Medicine, Animals, Recovery of Function, Muscle Contraction, Rats
Abstract

Muscle strains are one of the most common complaints treated by physicians. A muscle injury is typically diagnosed from the patient history and physical exam alone, however the clinical presentation can vary greatly depending on the extent of injury, the patient's pain tolerance, etc. In patients with muscle injury or muscle disease, assessment of muscle damage is typically limited to clinical signs, such as tenderness, strength, range of motion, and more recently, imaging studies. Biological markers, such as serum creatine kinase levels, are typically elevated with muscle injury, but their levels do not always correlate with the loss of force production. This is even true of histological findings from animals, which provide a "direct measure" of damage, but do not account for all the loss of function. Some have argued that the most comprehensive measure of the overall health of the muscle in contractile force. Because muscle injury is a random event that occurs under a variety of biomechanical conditions, it is difficult to study. Here, we describe an in vivo animal model to measure torque and to produce a reliable muscle injury. We also describe our model for measurement of force from an isolated muscle in situ. Furthermore, we describe our small animal MRI procedure.

Published
2011

87. Repeated Muscle Injury as a Presumptive Trigger for Chronic Masticatory Muscle Pain

Author

Dessem, Dean and Lovering, Richard M.

Subjects
Article Subject
Abstract

skeletal muscles sustain a significant loss of maximal contractile force after injury, but terminally damaged fibers can eventually be replaced by the growth of new muscle (regeneration), with full restoration of contractile force over time. After a second injury, limb muscles exhibit a smaller reduction in maximal force and reduced inflammation compared with that after the initial injury (i.e., repeated bout effect). In contrast, masticatory muscles exhibit diminished regeneration and persistent fibrosis, after a single injury; following a second injury, plasma extravasation is greater than after a single injury and maximal force is decreased more than after the initial injury. Thus, masticatory muscles do not exhibit a repeated bout effect and are instead increasingly damaged by repeated injury. We propose that the impaired ability of masticatory muscles to regenerate contributes to chronic muscle pain by leading to an accumulation of tissue damage, fibrosis, and a persistent elevation and prolonged membrane translocation of nociceptive channels such as P2X3 as well as enhanced expression of neuropeptides including CGRP within primary afferent neurons. These transformations prime primary afferent neurons for enhanced responsiveness upon subsequent injury thus triggering and/or exacerbating chronic muscle pain.

Published
2011
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96. NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation.

Author

Dongryeol Ryu, Hongbo Zhang, Ropelle, Eduardo R., Sorrentino, Vincenzo, Mázala, Davi A. G., Mouchiroud, Laurent, Marshall, Philip L., Campbell, Matthew D., Ali, Amir Safi, Knowels, Gary M., Bellemin, Stéphanie, Iyer, Shama R., Xu Wang, Gariani, Karim, Sauve, Anthony A., Cantó, Carles, Conley, Kevin E., Walter, Ludivine, Lovering, Richard M., and Chin, Eva R.

Subjects
DUCHENNE muscular dystrophy, NAD (Coenzyme), NEUROMUSCULAR diseases, LABORATORY rats, STEM cells, MESSENGER RNA
Abstract

The article discusses a study which found that nicotinamide adenine dinucleotide (NAD+) repletion is effective in improving muscle function in neuromuscular diseases like Duchene's muscular dystrophy (DMD) and delay both age-related and mdx muscle stem cell senescence. In the mice study, the correlations between the abundance of messenger ribonucleic acid (mRNA) transcripts related to mitochondrial biogenesis, the dystrophin-sarcoglycan complex, and NAD+ were observed.

Published
2016
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