Skeletal muscle fiber degeneration in mdx mice induced by electrical stimulation

Yoshida, Motoaki; Matsuzaki, Tetsuya; Date, Munehiro; Wada, Keiji

doi:10.1002/(sici)1097-4598(199711)20:11<1422::aid-mus10>3.0.co;2-3

Cited by 12 publications

(8 citation statements)

References 44 publications

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“…We expect that the process of muscle degeneration in DMD or mdx mice causes excess Ca 2ϩ to accumulate gradually in fibers after reaching a critical point in time, because their muscle fibers appear to function normally until a critical period is reached (47). In the case of mdx mice, the serum CK activity and K ϩ concentration do not increase until around age 7 days (Table 1).…”

Section: Discussionmentioning

confidence: 78%

“…In the case of mdx mice, the serum CK activity and K ϩ concentration do not increase until around age 7 days (Table 1). When muscle fibers, with high levels of accumulated calcium, receive stimulation, the fibers subsequently undergo extreme hypercontraction at the critical point (after age 7 days) and may lead to membrane rupture (47). At this moment, K ϩ may leak into the ECS and might produce the contraction of other muscle fibers around the ruptured fibers [potassium-induced contracture (27)].…”

Section: Discussionmentioning

confidence: 99%

“…The total calcium content of skeletal muscle fibers in DMD patients (3,4,24,29) and mdx mice (19,30,34) is higher than that found in normal muscle fibers. The causes leading to excess Ca 2ϩ influx into dystrophin-deficient muscle fibers are still unclear, although the following mechanisms have been proposed: 1) because dystrophin is thought to have a mechanical function, dystrophin-deficient muscle fiber membranes are predisposed to rupture (2,10); 2) Ca 2ϩ leak channels or stretch-activated channels open more easily in dystrophic myotubes, leading to poor Ca 2ϩ regulation (18); and 3) the function of L-type Ca 2ϩ channels is abnormal (12,47).…”

mentioning

confidence: 99%

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Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy

Yoshida

Yonetani²,

Shirasaki³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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The mdx mouse is an animal model for Duchenne muscular dystrophy. Mdx mice fed a 12% NaCl diet from birth up to 20 days of age (mdx-Na mice) had an approximately 50% reduction in serum creatine kinase (CK) activity compared with mdx mice fed a standard diet. Most notably, necrotic fibers in tibialis anterior (TA) muscle of mdx-Na mice were reduced by 99% and were similar in control mice. These mdx mice displayed significantly elevated blood Ca2+ and Na+ levels, while the total calcium content of their TA muscle was reduced to the level of control mice. In addition, mdx-Na mice had elevated zinc and magnesium contents in their TA muscle. These results suggest that elevated serum Na+ leads to Ca2+ extrusion from muscle via the Na+/Ca2+ exchanger causing a decrease in intracellular Ca2+ levels and an increase in blood Ca2+ levels. Extracellular Ca2+ and, in addition, Zn2+ and Mg2+ might also contribute to the stabilization of the cell membrane. Other possibilities explaining the surprisingly efficacious beneficial effect of dietary sodium exist and are discussed.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy

Yoshida

Yonetani²,

Shirasaki³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, overloading experiments induce degeneration and fragility of skeletal muscle in mdx mouse (Vilquin et al, 1998;Yoshida et al, 1997). This indicates that the skeletal muscle of mdx mouse is sensitive to overloading.…”

Section: Efficiency Of a Mutant Animal Modelmentioning

confidence: 99%

Spaceflight results in increase of thick filament but not thin filament proteins in the paramyosin mutant of Caenorhabditis elegans

Adachi

Takaya

Kuriyama

et al. 2008

Advances in Space Research

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We have investigated the effect of microgravity during spaceflight on body-wall muscle fiber size and muscle proteins in the paramyosin mutant of Caenorhabditis elegans.Both mutant and wild-type strains were subjected to 10 days of microgravity during spaceflight and compared to ground control groups. No significant change in muscle fiber size or quantity of the protein was observed in wild-type worms; where as atrophy of body-wall muscle and an increase in thick filament proteins were observed in the paramyosin mutant unc-15(e73) animals after spaceflight. We conclude that the mutant with abnormal muscle responded to microgravity by increasing the total amount of muscle protein in order to compensate for the loss of muscle function.

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“…The L-type Ca 2+ channel itself is reported to be activated by mechanical stretch [20]. The pathological importance of Ca 2+ influx via L-type Ca 2+ channel was also suggested for the electrical stimulation-induced damage of mdx skeletal fibres, as nifedipine effectively reduces the observed muscle damage [36].…”

Section: Mechanism Of Cell Damage In Sarcoglycan As-odn-treated Myotubesmentioning

confidence: 99%

Stretch-induced cell damage in sarcoglycan-deficient myotubes

Sampaolesi

Yoshida

Iwata

et al. 2001

Pfl�gers Archiv European Journal of Physiology

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Sarcoglycans (SGs) are components of the dystrophin-glycoprotein complex, genetic defects in which cause skeletal muscle dystrophy and cardiomyopathy in humans and animals. To obtain insight into the roles of SGs, we characterized properties of myotubes prepared from cells of the rat L6 line or primary myoblast cultures of rat gastrocnemius muscle that were made SG-deficient by treatment with antisense oligodeoxynucleotides (AS-ODNs). Immunoblot and immunoprecipitation analyses revealed that dystrophin and its remaining associated proteins were tightly associated in these cells despite SG deficiency. 45Ca2+ influx into SG AS-ODN-treated L6 myotubes under resting conditions was significantly higher (1.7-fold at 6 min) than in controls, suggesting that Ca2+ influx is activated in these SG-deficient myotubes. When these cells were subjected to cyclic elongation of up to 20% for 1 h, a marked increase in creatine phosphokinase (CK) release into the medium was observed. Nifedipine, tranilast, FK506 and E64 or intracellular loading with 1,2-bis(2-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid, tetrakis(acetoxymethyl)ester (BAPTA/AM) reduced the stretch-induced CK release; a raised extracellular [Ca2+] increased CK release. The stretch-induced damage to SG-deficient myotubes thus appears to be caused by alterations in cell Ca2+ homeostasis. A similar abnormality in Ca2+ handling has been reported for myoctes from mdx mice or dystrophin-deficient patients, in whom SGs are also greatly reduced or absent. Thus it is possible that SG deficiency may play a critical role in the pathology of dystrophin-deficient muscle.

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Skeletal muscle fiber degeneration in mdx mice induced by electrical stimulation

Cited by 12 publications

References 44 publications

Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy

Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy

Spaceflight results in increase of thick filament but not thin filament proteins in the paramyosin mutant of Caenorhabditis elegans

Stretch-induced cell damage in sarcoglycan-deficient myotubes

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