Evidence ofmdx mouse skeletal muscle fragility in vivo by eccentric running exercise

Vilquin, Jean‐Thomas; Brussee, Valentine; Asselin, Isabelle; Kinoshita, Ikuo; Gingras, M.; Tremblay, Jacques P.

doi:10.1002/(sici)1097-4598(199805)21:5<567::aid-mus2>3.0.co;2-6

Cited by 109 publications

(73 citation statements)

References 50 publications

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“…Bartolomucci et al (2009) reported that mice exposed to stress showed decreased locomotor activity during the active phase. In our results, blood creatine kinase activity, which is generally considered to increase in blood after exercise such as running (Vilquin et al, 1998), was significantly lower in the group exposed to social isolation stress (Table 3), indicating the possibility that the locomotion was lower. That is, lower energy consumption under the social isolation stress, could be one of the reasons for the increase in the body, liver and visceral fat weights under the social isolation stress.…”

Section: Resultsmentioning

confidence: 49%

Social isolation stress induces hepatic hypertrophy in C57BL/6J mice

et al. 2012

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-We previously reported that social isolation stimulated a stress response leading to increasing plasma corticosterone level and disruption of the hepatic lipid metabolism-related pathway, without changing body and organ weights, in mice after 4 weeks of social isolation stress, compared with the grouped-housing control (5 mice/cage). In this study, we evaluated the effects of social isolation stress for an extended period on physiologic changes in male C57BL/6J mice. Plasma corticosterone was reduced after 13 weeks, indicating mice might adapt to social isolation stress. However, body and visceral fat weights were significantly increased in combination with hepatic hypertrophy, and significant decreases in levels of triglyceride and adiponectin in plasma were observed. In conclusion, it is tempting to speculate that mice exposed to social isolation stress for 13 continuous weeks could be at an increased risk of overweight with hepatic hypertrophy. Our results also imply that physiological changes, at least fatty acid metabolism, under stress exposure might be an important factor when evaluating the chronic effects of environmental chemicals.

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Section: Resultsmentioning

confidence: 49%

Social isolation stress induces hepatic hypertrophy in C57BL/6J mice

et al. 2012

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“…This increase is mild when compared with other mouse models of muscular dystrophy (Sonnemann et al, 2006). Finally, we evaluated whether talin 1-deficient muscles were more susceptible to muscle fiber damage when subjected to exercise, as has been observed in other models for muscular dystrophy (Armstrong et al, 1983;Hamer et al, 2002;McNeil and Khakee, 1992;Vilquin et al, 1998). EBD was injected into 5-to 6-month-old mice and, 1 hour after injection, mice were run on a treadmill for 30 minutes.…”

Section: Research Articlementioning

confidence: 78%

Progressive myopathy and defects in the maintenance of myotendinous junctions in mice that lack talin 1 in skeletal muscle

Conti

Felder²,

Monkley

et al. 2008

Development

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The development and function of skeletal muscle depend on molecules that connect the muscle fiber cytoskeleton to the extracellular matrix (ECM). β1 integrins are ECM receptors in skeletal muscle, and mutations that affect the α7β1 integrin cause myopathy in humans. In mice, β1 integrins control myoblast fusion, the assembly of the muscle fiber cytoskeleton, and the maintenance of myotendinous junctions (MTJs). The effector molecules that mediate β1 integrin functions in muscle are not known. Previous studies have shown that talin 1 controls the force-dependent assembly of integrin adhesion complexes and regulates the affinity of integrins for ligands. Here we show that talin 1 is essential in skeletal muscle for the maintenance of integrin attachment sites at MTJs. Mice with a skeletal muscle-specific ablation of the talin 1 gene suffer from a progressive myopathy. Surprisingly, myoblast fusion and the assembly of integrin-containing adhesion complexes at costameres and MTJs advance normally in the mutants. However, with progressive ageing, the muscle fiber cytoskeleton detaches from MTJs. Mechanical measurements on isolated muscles show defects in the ability of talin 1-deficient muscle to generate force. Collectively, our findings show that talin 1 is essential for providing mechanical stability to integrin-dependent adhesion complexes at MTJs, which is crucial for optimal force generation by skeletal muscle.

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“…Evans blue dye (EBD; SigmaAldrich, St. Louis, Missouri, USA; 10 mg/ml PBS, 50 µl/10 g body weight) was injected into the retro-orbital vein; 12 to 24 hours after injection, mice were killed, skinned, and visually inspected for blue coloration as described (16). Cryosections of gastrocnemius muscle were examined by confocal microscopy.…”

Section: Methodsmentioning

confidence: 99%

Impaired neuromuscular transmission and skeletal muscle fiber necrosis in mice lacking Na/Ca exchanger 3

Sokolow¹,

Manto²,

Gailly³

et al. 2004

J. Clin. Invest.

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We produced and analyzed mice deficient for Na/Ca exchanger 3 (NCX3), a protein that mediates cellular Ca2+ efflux (forward mode) or Ca2+ influx (reverse mode) and thus controls intracellular Ca2+ concentration. NCX3-deficient mice (Ncx3–/–) present a skeletal muscle fiber necrosis and a defective neuromuscular transmission, reflecting the absence of NCX3 in the sarcolemma of the muscle fibers and at the neuromuscular junction. The defective neuromuscular transmission is characterized by the presence of electromyographic abnormalities, including low compound muscle action potential amplitude, a decremental response at low-frequency nerve stimulation, an incremental response, and a prominent postexercise facilitation at high-frequency nerve stimulation, as well as neuromuscular blocks. The analysis of quantal transmitter release in Ncx3–/– neuromuscular junctions revealed an important facilitation superimposed on the depression of synaptic responses and an elevated delayed release during high-frequency nerve stimulation. It is suggested that Ca2+ entering nerve terminals is cleared relatively slowly in the absence of NCX3, thereby enhancing residual Ca2+ and evoked and delayed quantal transmitter release during repetitive nerve stimulation. Our findings indicate that NCX3 plays an important role in vivo in the control of Ca2+ concentrations in the skeletal muscle fibers and at the neuromuscular junction

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Evidence ofmdx mouse skeletal muscle fragility in vivo by eccentric running exercise

Cited by 109 publications

References 50 publications

Social isolation stress induces hepatic hypertrophy in C57BL/6J mice

Social isolation stress induces hepatic hypertrophy in C57BL/6J mice

Progressive myopathy and defects in the maintenance of myotendinous junctions in mice that lack talin 1 in skeletal muscle

Impaired neuromuscular transmission and skeletal muscle fiber necrosis in mice lacking Na/Ca exchanger 3

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