Physiological properties of dissociated muscle fibres obtained from innervated and denervated adult rat muscle.

Bekoff, Anne; Betz, William J.

doi:10.1113/jphysiol.1977.sp011988

Cited by 138 publications

(101 citation statements)

References 18 publications

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“…We adopted an enzymatic technique that enabled the isolation of physiological skeletal myofibers from rodent flexor digitorum brevis (FDB) muscle, which consists of the shortest myofibers in the body (14). We could establish a primary culture system for the myofibers from rat FDB muscles (11, 15 -17).…”

Section: Primary Cultured Skeletal Myofibers Reproduce Statin Myotoximentioning

confidence: 99%

Mechanism of Statin-Induced Rhabdomyolysis

Sakamoto

Kimura

2013

J Pharmacol Sci

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Abstract. Statins, a group of drugs used for the treatment of hypercholesterolemia, have adverse effects on skeletal muscle. The symptoms of these effects range from slight myalgia to severe rhabdomyolysis. The number of patients currently taking statins is estimated to be several millions worldwide. However, the mechanism of statins' myotoxic effects is unclear. Statins inhibit biosynthesis of mevalonate, a rate-limiting step of cholesterol synthesis, by inhibiting HMG-CoA reductase. Mevalonate is also an essential precursor for producing isoprenoids such as farnesylpyrophosphate and geranylgeranylpyrophosphate. These isoprenoids are especially important for anchoring small GTPases to the membrane before they function; e.g., Ras GTPases modulate proliferation and apoptosis, Rho GTPases control cytoskeleton formation, and Rab GTPases are essential for intracellular vesicle trafficking. Inactivation of these small GTPases alters cellular functions. Recently, we successfully reproduced statin-induced myotoxicity in culture dishes using in vitro skeletal muscle systems (e.g., skeletal myotubes and myofibers). This review summarizes our findings that statins induce depletion of isoprenoids and inactivation of small GTPases, especially Rab, which are critical for statin-induced myotoxicity. Although further study is required, our findings may contribute to the prevention and treatment of statins' adverse effects on skeletal muscle and development of safer anti-hypercholesterolemia drugs.

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Section: Primary Cultured Skeletal Myofibers Reproduce Statin Myotoximentioning

confidence: 99%

Mechanism of Statin-Induced Rhabdomyolysis

Sakamoto

Kimura

2013

J Pharmacol Sci

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“…17,31,32 Briefly, mice were killed by cervical dislocation and entire EDL, TA and soleus muscles, including tendons, were removed. Muscles were digested for 60-90 min in 0.2% collagenase in DMEM at 35°C, and then separated into single fibres by trituration.…”

Section: Single Myofibre Preparationmentioning

confidence: 99%

Transplanted primary neonatal myoblasts can give rise to functional satellite cells as identified using the Myf5nlacZl+ mouse

et al. 2001

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Myoblast transplantation is a potential therapeutic approach for the genetic modification of host skeletal muscle tissue. To be considered an effective, long-lived method of delivery, however, it is essential that at least a proportion of the transplanted cells also retain their proliferative potential. We sought to investigate whether transplanted neonatal myoblasts can contribute to the satellite cell compartment of adult skeletal muscle by using the Myf5 nlacZ/+ mouse. The Myf5 nlacZ/+ mouse has nlacZ targeted to the Myf5 locus resulting in ␤-galactosidase activity in quiescent satellite cells. Following transplantation, ␤-galactosidase-labelled nuclei were detected in host muscles, showing that donor

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“…Intact skeletal muscle fibres were dissociated from the flexor digitorum brevis (FDB) muscle from 2-week-old wildtype and mdx mice following the procedure described by Bekoff & Betz (1977 Electrophysiological methods Single-channel activity wvas recorded from cell-attached patches using the technique described by Hamill, Marty, Neher, Sakmann & Sigworth (1981). Patch (Colquhoun & Sigworth, 1983 (Chatfield, 1983 enclose 50% of the data points.…”

Section: Muscle Cell Preparationmentioning

confidence: 99%

Mechanosensitive ion channels in skeletal muscle from normal and dystrophic mice.

Franco‐Obregón

Lansman

1994

The Journal of Physiology

136

106

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1. We examined the activity of single mechanosensitive ion channels in recordings from cell-attached patches on myoblasts, differentiated myotubes and acutely isolated skeletal muscle fibres from wild-type and mdx and dy mutant mice. The experiments were concerned with the role of these channels in the pathophysiology of muscular dystrophy. 2. The predominant form of channel activity recorded with physiological saline in the patch electrode arose from an -25 pS mechanosensitive ion channel. Channel activity was similar in undifferentiated myoblasts isolated from all three strains of mice. By contrast, channel activity in mdx myotubes was -3-4 times greater than in either wildtype or dy myotubes and arose from a novel mode of mechanosensitive gating. 3. Single mechanosensitive channels in acutely isolated flexor digitorum brevis fibres had properties indistinguishable from those of muscle cells grown in tissue culture. The channel open probability in mdx fibres was -2 times greater than the activity recorded from wild-type fibres. The overall level of activity in fibres, however, was roughly an order of magnitude smaller than in myoblasts or myotubes. 4. Histological examination of the flexor digitorum brevis fibres from mdx mice showed no evidence of myonecrosis or regenerating fibres, suggesting that the elevated channel activity in dystrophin-deficient muscle precedes the onset of fibre degeneration. 5. An early step in the dystrophic process of the mdx mouse, which leads to pathophysiological Ca2+ entry, may be an alteration in the mechanisms that regulate mechanosensitive ion channel activity.

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Physiological properties of dissociated muscle fibres obtained from innervated and denervated adult rat muscle.

Cited by 138 publications

References 18 publications

Mechanism of Statin-Induced Rhabdomyolysis

Mechanism of Statin-Induced Rhabdomyolysis

Transplanted primary neonatal myoblasts can give rise to functional satellite cells as identified using the Myf5nlacZl+ mouse

Mechanosensitive ion channels in skeletal muscle from normal and dystrophic mice.

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