Developmental regulation of mechanosensitive calcium channels in skeletal muscle from normal and
            <i>mdx</i>
            mice

Haws, C. M.; Lansman, Jeffry B.

doi:10.1098/rspb.1991.0105

Cited by 37 publications

(10 citation statements)

References 12 publications

(5 reference statements)

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“…A striking exception was in recordings from mdx myotubes, which frequently showed a form of activity where channel open probability approached unity under resting conditions (Fig. 2, third trace in the second column; see also Franco & Lansman, 1990a (Haws & Lansman, 1991). Although we could not detect any differences between normal and mdx FDB fibres in channel density, it is possible that there are differences in the spatial localization of channels not easily detected by recordings from cell-attached patches.…”

Section: Determination Of the Mechanical Strength Of Normal And Dystrmentioning

confidence: 69%

“…The levels of channel activity were roughly an order of magnitude lower in wild-type and mdx fibres than in myotubes. The box-plot analysis (see Methods) showed, however, that the median value of channel open probability in mdx fibres is greater than in wild-type fibres and the distribution of open probabilities falls towards higher values (see also Haws & Lansman, 1991). The results in Fig.…”

Section: Determination Of the Mechanical Strength Of Normal And Dystrmentioning

confidence: 74%

“…In a previous study of mechanosensitive channel activity in mdx fibres (Haws & Lansman, 1991), we suggested that the small fraction of patches showing high levels of activity in mdx fibres may represent sites at which there is a localized influx of extracellular Ca2+ which could be sufficient to produce focal damage. If such focal lesions accumulated, they could produce a much larger disruption of sarcolemmal integrity.…”

Section: Discussionmentioning

confidence: 91%

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

Franco‐Obregón

Lansman

1994

The Journal of Physiology

132

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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Section: Determination Of the Mechanical Strength Of Normal And Dystrmentioning

confidence: 69%

Section: Determination Of the Mechanical Strength Of Normal And Dystrmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 91%

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

Franco‐Obregón

Lansman

1994

The Journal of Physiology

132

106

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“…Functionally abnormal calcium channels have been found in myotubes grown from mdx mice and DMD humans (Fong et al 1990; Franco & Lansman, 1990) and result in calcium entry when the myotubes are at rest. However, these channels have not been found in dystrophin deficient adult mdx muscle cells (Haws & Lansman, 1991). In the adult mdx mice between 2-5 weeks of age the proximal limb muscles undergo a process of degeneration which affects up to 100 % of the fibres in some muscles (Carnwath & Shotton, 1987).…”

Section: Introductionmentioning

confidence: 99%

Membrane potential, resting calcium and calcium transients in isolated muscle fibres from normal and dystrophic mice.

Head

1993

The Journal of Physiology

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SUMMARY1. Single skeletal muscle fibres were enzymatically isolated from the flexor digitorum brevis muscles (FDB) of dystrophic mdx and control C57BL/10 mice aged 3-9 weeks. In this age range the majority (> 95%) of the mdx fibres were morphologically normal.2. There was no significant difference between the resting membrane potential (RMP) of mdx and control mice, -71P2+ 1-21 (n = 26) and -70-6+ 1-15 mV (n = 42), respectively.3. At RMP more negative than -60 mV the resting calcium (recorded with fura-2, free acid ionophoresed into cell) in the dystrophic mdx cells was not significantly different from the normal animals, 45-7 + 4-1 (n = 10) and 46-2 +39 nm (n = 9), respectively.4. The resting cytosolic calcium concentration was measured simultaneously with the RMP. At RMP between -60 to -17 mV there was an increase in the resting calcium concentration in both mdx and control ranging from 79-3 to 252 nm. This increase was most probably due to the activation of the slow calcium current.5. Fura-2 calcium transients were produced via single action potential stimulation using an intracellular microelectrode both to stimulate the cell and record potential changes. There was no significant difference between the rise time (Tn) or half-decay time (Ti) at 22°C of the calcium transient in response to a single action potential in mdx compared to normal animals, 5-9 + 0-34 (n = 8) and 5-4 + 0-36 ms (n = 7); 39-5 + 2-9 (n = 8) and 40 75 + 3 7 ms (n = 7), respectively.6. In conclusion it appears that over the age range 3-9 weeks the absence of dystrophin does not affect the RMP, resting calcium or calcium transient parameters of morphologically normal FDB mtdx fibres.

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“…SACs are non-selective ion channels that are present in a huge variety of cells and organisms, where they participate in mechanotransduction, converting membrane stretch into electrical Ca 2+ , K + and Na + current across the plasma membrane, and biochemical signals (Ambudkar, 2006;Sachs and Morris, 1998). In particular, SAC expression and activity are prevalent in neonatal skeletal muscle tissue and undifferentiated myoblasts, and decline as myoblasts mature and fuse into myotubes (Formigli et al, 2007b;Haws and Lansman, 1991). Moreover, the inhibition of these channels with several pharmacological compounds, including gadolinium chloride (GdCl 3 ), streptomycin and the spider venom toxin (GsMTx4), has been shown to suppress the expression of the typical myogenic markers and the myoblast-myotube transition, suggesting that SAC activation may lead to increased Ca 2+ entries necessary for skeletal muscle differentiation (Formigli et al, 2007b;Wedhas et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Regulation of transient receptor potential canonical channel 1 (TRPC1) by sphingosine 1-phosphate in C2C12 myoblasts and its relevance for a role of mechanotransduction in skeletal muscle differentiation

Formigli

Sassoli

Squecco

et al. 2009

Journal of Cell Science

102

108

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Transient receptor potential canonical (TRPC) channels provide cation and Ca2+ entry pathways, which have important regulatory roles in many physio-pathological processes, including muscle dystrophy. However, the mechanisms of activation of these channels remain poorly understood. Using siRNA, we provide the first experimental evidence that TRPC channel 1 (TRPC1), besides acting as a store-operated channel, represents an essential component of stretch-activated channels in C2C12 skeletal myoblasts, as assayed by whole-cell patch-clamp and atomic force microscopic pulling. The channel's activity and stretch-induced Ca2+ influx were modulated by sphingosine 1-phosphate (S1P), a bioactive lipid involved in satellite cell biology and tissue regeneration. We also found that TRPC1 was functionally assembled in lipid rafts, as shown by the fact that cholesterol depletion resulted in the reduction of transmembrane ion current and conductance. Association between TRPC1 and lipid rafts was increased by formation of stress fibres, which was elicited by S1P and abolished by treatment with the actin-disrupting dihydrocytochalasin B, suggesting a role for cytoskeleton in TRPC1 membrane recruitment. Moreover, TRPC1 expression was significantly upregulated during myogenesis, especially in the presence of S1P, implicating a crucial role for TRPC1 in myoblast differentiation. Collectively, these findings may offer new tools for understanding the role of TRPC1 and sphingolipid signalling in skeletal muscle regeneration and provide new therapeutic approaches for skeletal muscle disorders.

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Developmental regulation of mechanosensitive calcium channels in skeletal muscle from normal and mdx mice

Cited by 37 publications

References 12 publications

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

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

Membrane potential, resting calcium and calcium transients in isolated muscle fibres from normal and dystrophic mice.

Regulation of transient receptor potential canonical channel 1 (TRPC1) by sphingosine 1-phosphate in C2C12 myoblasts and its relevance for a role of mechanotransduction in skeletal muscle differentiation

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