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Journal articles on the topic 'R6-2 skeletal muscle'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Miranda, Daniel R., Monica Wong, Shannon H. Romer, et al. "Progressive Cl− channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington’s mice." Journal of General Physiology 149, no. 1 (2016): 55–74. http://dx.doi.org/10.1085/jgp.201611603.

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Huntington’s disease (HD) patients suffer from progressive and debilitating motor dysfunction. Previously, we discovered reduced skeletal muscle chloride channel (ClC-1) currents, inwardly rectifying potassium (Kir) channel currents, and membrane capacitance in R6/2 transgenic HD mice. The ClC-1 loss-of-function correlated with increased aberrant mRNA processing and decreased levels of full-length ClC-1 mRNA (Clcn1 gene). Physiologically, the resulting muscle hyperexcitability may help explain involuntary contractions of HD. In this study, the onset and progression of these defects are investi

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2

Miranda, Daniel R., Eric Reed, Abdulrahman Jama, et al. "Mechanisms of altered skeletal muscle action potentials in the R6/2 mouse model of Huntington’s disease." American Journal of Physiology-Cell Physiology 319, no. 1 (2020): C218—C232. http://dx.doi.org/10.1152/ajpcell.00153.2020.

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Huntington’s disease (HD) patients suffer from progressive and debilitating motor dysfunction for which only palliative treatment is currently available. Previously, we discovered reduced skeletal muscle Cl− channel (ClC-1) and inwardly rectifying K+ channel (Kir) currents in R6/2 HD transgenic mice. To further investigate the role of ClC-1 and Kir currents in HD skeletal muscle pathology, we measured the effect of reduced ClC-1 and Kir currents on action potential (AP) repetitive firing in R6/2 mice using a two-electrode current clamp. We found that R6/2 APs had a significantly lower peak amp

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3

Braubach, Peter, Murat Orynbayev, Zoita Andronache, et al. "Altered Ca2+ signaling in skeletal muscle fibers of the R6/2 mouse, a model of Huntington’s disease." Journal of General Physiology 144, no. 5 (2014): 393–413. http://dx.doi.org/10.1085/jgp.201411255.

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Huntington’s disease (HD) is caused by an expanded CAG trinucleotide repeat within the gene encoding the protein huntingtin. The resulting elongated glutamine (poly-Q) sequence of mutant huntingtin (mhtt) affects both central neurons and skeletal muscle. Recent reports suggest that ryanodine receptor–based Ca2+ signaling, which is crucial for skeletal muscle excitation–contraction coupling (ECC), is changed by mhtt in HD neurons. Consequently, we searched for alterations of ECC in muscle fibers of the R6/2 mouse, a mouse model of HD. We performed fluorometric recordings of action potentials (A

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4

Hayashi, Yoshihiro, Takaaki Ikata, Hiroaki Takai, Shinjiro Takata, Takayuki Sogabe, and Keiko Koga. "Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation." Journal of Applied Physiology 82, no. 3 (1997): 732–37. http://dx.doi.org/10.1152/jappl.1997.82.3.732.

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Hayashi, Yoshihiro, Takaaki Ikata, Hiroaki Takai, Shinjiro Takata, Takayuki Sogabe, and Keiko Koga. Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation. J. Appl. Physiol. 82(3): 732–737, 1997.—This study examined the time course of recovery from nerve injury on energy state assessed by phosphorus-31 magnetic resonance spectroscopy and local circulation dynamics by fluorine-19 magnetic resonance spectroscopy in skeletal muscles of rats. The hindlimb muscles that had undergone unilateral sciatic nerve compression for 2 wk (CN) were compared with sham-

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5

Magnusson-Lind, Anna, Marcus Davidsson, Edina Silajdžić, et al. "Skeletal Muscle Atrophy in R6/2 Mice – Altered Circulating Skeletal Muscle Markers and Gene Expression Profile Changes." Journal of Huntington's Disease 3, no. 1 (2014): 13–24. http://dx.doi.org/10.3233/jhd-130075.

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6

She, Pengxiang, Zhiyou Zhang, Deanna Marchionini, et al. "Molecular characterization of skeletal muscle atrophy in the R6/2 mouse model of Huntington's disease." American Journal of Physiology-Endocrinology and Metabolism 301, no. 1 (2011): E49—E61. http://dx.doi.org/10.1152/ajpendo.00630.2010.

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Huntington's disease (HD), a neurodegenerative disorder caused by mutant huntingtin, is characterized by a catabolic phenotype. To determine the mechanisms underlying muscle wasting, we examined key signal transduction pathways governing muscle protein metabolism, apoptosis, and autophagy in R6/2 mice, a well-characterized transgenic model of HD. R6/2 mice exhibited increased adiposity, elevated energy expenditure, and decreased body weight and lean mass without altered food intake. Severe skeletal muscle wasting accounted for a majority of the weight loss. Protein synthesis was unexpectedly i

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7

Braubach, P., Z. Andronache, A. Riecker, et al. "A21 Altered calcium kinetics in skeletal muscle fibres of the R6/2 mouse model of HD." Journal of Neurology, Neurosurgery & Psychiatry 81, Suppl 1 (2010): A7.1—A7. http://dx.doi.org/10.1136/jnnp.2010.222570.21.

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8

Kojer, Kerstin, Tanja Hering, Chantal Bazenet, et al. "Huntingtin Aggregates and Mitochondrial Pathology in Skeletal Muscle but not Heart of Late-Stage R6/2 Mice." Journal of Huntington's Disease 8, no. 2 (2019): 145–59. http://dx.doi.org/10.3233/jhd-180324.

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9

Hering, T., K. Kojer, N. Birth, et al. "D03 Mitochondrial Biogenesis, And Respiratory Chain Assembly And Function, In Skeletal Muscle Of The R6/2 Mouse Model And Human Huntington's Disease." Journal of Neurology, Neurosurgery & Psychiatry 85, Suppl 1 (2014): A32. http://dx.doi.org/10.1136/jnnp-2014-309032.95.

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10

Wackler, P., T. Lenk, T. Hering, M. Orth, GB Landwehrmeyer, and KS Lindenberg. "B21 Decreased expression and reduced translocation to the sarcolemma of the insulin-sensitive glucose transporter GLUT4 in skeletal muscle of R6/2 MICE." Journal of Neurology, Neurosurgery & Psychiatry 83, Suppl 1 (2012): A12.1—A12. http://dx.doi.org/10.1136/jnnp-2012-303524.37.

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11

Tupling, A. R., E. Bombardier, R. D. Stewart, C. Vigna, and A. E. Aqui. "Muscle fiber type-specific response of Hsp70 expression in human quadriceps following acute isometric exercise." Journal of Applied Physiology 103, no. 6 (2007): 2105–11. http://dx.doi.org/10.1152/japplphysiol.00771.2007.

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To investigate the time course of fiber type-specific heat shock protein 70 (Hsp70) expression in human skeletal muscle after acute exercise, 10 untrained male volunteers performed single-legged isometric knee extensor exercise at 60% of their maximal voluntary contraction (MVC) with a 50% duty cycle (5-s contraction and 5-s relaxation) for 30 min. Muscle biopsies were collected from the vastus lateralis before (Pre) exercise in the rested control leg (C) and immediately after exercise (Post) in the exercised leg (E) only and on recovery days 1 (R1), 2 (R2), 3 (R3), and 6 (R6) from both legs.

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12

Hering, Tanja, Peter Braubach, G. Bernhard Landwehrmeyer, Katrin S. Lindenberg, and Werner Melzer. "Fast-to-Slow Transition of Skeletal Muscle Contractile Function and Corresponding Changes in Myosin Heavy and Light Chain Formation in the R6/2 Mouse Model of Huntington’s Disease." PLOS ONE 11, no. 11 (2016): e0166106. http://dx.doi.org/10.1371/journal.pone.0166106.

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13

Romer, Shannon H., Sabrina Metzger, Kristiana Peraza, et al. "A mouse model of Huntington’s disease shows altered ultrastructure of transverse tubules in skeletal muscle fibers." Journal of General Physiology 153, no. 4 (2021). http://dx.doi.org/10.1085/jgp.202012637.

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Huntington’s disease (HD) is a fatal and progressive condition with severe debilitating motor defects and muscle weakness. Although classically recognized as a neurodegenerative disorder, there is increasing evidence of cell autonomous toxicity in skeletal muscle. We recently demonstrated that skeletal muscle fibers from the R6/2 model mouse of HD have a decrease in specific membrane capacitance, suggesting a loss of transverse tubule (t-tubule) membrane in R6/2 muscle. A previous report also indicated that Cav1.1 current was reduced in R6/2 skeletal muscle, suggesting defects in excitation–co

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14

Sjögren, Marie, Ana I. Duarte, Andrew C. McCourt, Liliya Shcherbina, Nils Wierup, and Maria Björkqvist. "Ghrelin rescues skeletal muscle catabolic profile in the R6/2 mouse model of Huntington’s disease." Scientific Reports 7, no. 1 (2017). http://dx.doi.org/10.1038/s41598-017-13713-5.

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15

She, Pengxiang, Zhiyou Zhang, Deanna Marchionini, Thomas Jetton, Charles Lang, and Christopher Lynch. "Molecular Characterization of Skeletal Muscle Atrophy in the R6/2 Mouse Model of Huntington's Disease." FASEB Journal 25, S1 (2011). http://dx.doi.org/10.1096/fasebj.25.1_supplement.1059.7.

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16

Lindenberg, K. S., Z. Andronache, M. Orynbayev, et al. "Morphological and functional changes in skeletal muscle of the Huntington's disease mouse model R6/2 suggest selective changes in fast-twitch fibres." Aktuelle Neurologie 35, S 01 (2008). http://dx.doi.org/10.1055/s-0028-1086923.

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17

Paré, Marie-France, та Bernard J. Jasmin. "Chronic 5-Aminoimidazole-4-Carboxamide-1-β-d-Ribofuranoside Treatment Induces Phenotypic Changes in Skeletal Muscle, but Does Not Improve Disease Outcomes in the R6/2 Mouse Model of Huntington’s Disease". Frontiers in Neurology 8 (27 вересня 2017). http://dx.doi.org/10.3389/fneur.2017.00516.

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