Calcium currents in normal and dystrophic human skeletal muscle cells in culture

Rivet, Michèle; Cognard, Christian; Rideau, Y; Duport, G; Raymond, Guy

doi:10.1016/0143-4160(90)90026-q

Cited by 25 publications

(10 citation statements)

References 28 publications

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“…In contrast to the cardiac L_type channel, Ca¥ current passed by the heterologously expressed skeletal muscle isoform did not show a U-shaped dependence of the inactivation time constant on voltage (Gonzalez et al 1995). In addition, substituting Ba¥ for Ca¥ caused relatively minor kinetic changes of the current in primary cultured skeletal myocytes, although the contribution of a Ca¥-dependent component to the slow decline could not be ruled out (Cognard et al 1986;Beam & Knudson, 1988;Rivet et al 1990). In frog skeletal muscle fibres, Almers et al (1981) identified a decline of the current which was correlated with its size even under conditions of very strong internal calcium buffering.…”

Section: Discussionmentioning

confidence: 99%

“…The characteristics of this type of inactivation have not yet been fully determined in any skeletal muscle preparation and particularly little information is available from human preparations which have recently attracted attention due to the discovery of L_type Ca¥ channelrelated diseases (Jurkat-Rott et al 1994;Ptacek et al 1994;Monnier et al 1997). A few studies describe voltagedependent activation and inactivation in human muscle cells (Rivet et al 1990(Rivet et al , 1992Garcia et al 1992;Sipos et al 1995;Lehmann-Horn et al 1995;Jurkat-Rott et al 1998) but no data are available on the dynamics of the transition to and the recovery from the inactive state(s). The purpose of the present investigation was to characterize these processes in cultured myocytes.…”

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confidence: 99%

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Kinetics of inactivation and restoration from inactivation of the L‐type calcium current in human myotubes

Harasztosi

Sipos

Kovács

et al. 1999

The Journal of Physiology

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1. Inactivation and recovery kinetics of L_type calcium currents were measured in myotubes derived from satellite cells of human skeletal muscle using the whole cell patch clamp technique. 2. The time course of inactivation at potentials above the activation threshold was obtained from the decay of the current during 15 s depolarizing pulses. At subthreshold potentials, prepulses of different durations, followed by +20 mV test pulses, were used. The time course could be well described by single exponential functions of time. The time constant decreased from 17·8 ± 7·5 s at −30 mV to 1·78 ± 0·15 s at +50 mV. 3. Restoration from inactivation caused by 15 s depolarization to +20 mV was slowed by depolarization in the restoration interval. The time constant increased from 1·11 ± 0·17 s at −90 mV to 7·57 ± 2·54 s at −10 mV. 4. Restoration showed different kinetics depending on the duration of the conditioning depolarization. While the time constant was similar at restoration potentials of −90 and −50 mV after a 1 s conditioning prepulse, it increased with increasing prepulse duration at −50 mV and decreased at −90 mV. 5. The experiments showed that the rates of inactivation and restoration of the L_type calcium current in human myotubes were not identical when observed at the same potential. The results indicate the presence of more than one inactivated state and point to different voltage-dependent pathways for inactivation and restoration.8422

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Kinetics of inactivation and restoration from inactivation of the L‐type calcium current in human myotubes

Harasztosi

Sipos

Kovács

et al. 1999

The Journal of Physiology

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“…Culture and co-culture of human skeletal muscle cells As previously described (Rivet et al 1990), primary cultures of human skeletal muscle cells were initiated from satellite cells of muscle samples obtained during orthopaedic surgery (with the agreement of the Comité pour l'Ethique Médicale du Centre Hospitalier Régional de Poitiers and in accordance with French institutional guidelines) from patients without a neuromuscular disorder (n = 35) and DMD patients (n = 16). Informed consent was given in writing before surgery by the subject or his relatives, and all work conformed with the Declaration of Helsinki.…”

Section: Methodsmentioning

confidence: 99%

“…Since one of the functions of calcium channel molecules is to transfer calcium ions into the cells, this process could be one of the potential candidates for contributing to the calcium entry and accumulation in DMD cells. In vitro studies on aneurally cultured cells have shown the existence of at least two types of voltage-dependent calcium current (T and L); their characteristics have been extensively studied in normal (Rivet et al 1990(Rivet et al , 1992Garcia et al 1992;Sipos et al 1997;Morill et al 1998;Harasztosi et al 1999) and DMD muscle cells (Rivet et al 1990), but no obvious differences in the voltage dependence and kinetics of these calcium currents have been observed, as expected from cells in which the resting intracellular calcium concentration remained similar. Consequently, in order to address a possible involvement of such calcium channels in the detected intracellular calcium concentration elevation, investigations in co-cultured human muscle cells were essential despite the low availability of DMD biopsies.…”

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confidence: 99%

Calcium currents and transients in co‐cultured contracting normal and Duchenne muscular dystrophy human myotubes

Imbert

Vandebrouck

Duport

et al. 2001

The Journal of Physiology

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1. The goal of the present study was to investigate differences in calcium movements between normal and Duchenne muscular dystrophy (DMD) human contracting myotubes co-cultured with explants of rat spinal cord with attached dorsal root ganglia. Membrane potential, variations of intracellular calcium concentration and T-and L-type calcium currents were recorded. Further, a descriptive and quantitative study by electron microscopy of the ultrastructure of the co-cultures was carried out.2. The resting membrane potential was slightly less negative in DMD (_61.4 ± 1.1 mV) than in normal myotubes (_65.5 ± 0.9 mV). Both types of myotube displayed spontaneous action potentials (mean firing frequency, 0.42 and 0.16 Hz, respectively), which triggered spontaneous calcium transients measured with Indo-1.3. The time integral under the spontaneous Ca 2+ transients was significantly greater in DMD myotubes (97 ± 8 nM s) than in normal myotubes (67 ± 13 nM s).4. The L-and T-type current densities estimated from patch-clamp recordings were smaller in DMD cells (2.0 ± 0.5 and 0.90 ± 0.19 pA pF _1 , respectively) than in normal cells (3.9 ± 0.7 and 1.39 ± 0.30 pA pF _1 , respectively). The voltage-dependent inactivation relationships revealed a shift in the conditioning potentialat which inactivation is half-maximal (V h,0.5 ) of the T-and L-type currents towards less negative potentials, from _72.1 ± 0.7 and _53.7 ± 1.5 mV in normal cells to _61.9 ± 1.4 and _29.2 ± 1.4 mV in DMD cells, respectively.6. Both descriptive and quantitative studies by electron microscopy suggested a more advanced development of DMD myotubes as compared to normal ones. This conclusion was supported by the significantly larger capacitance of the DMD myotubes (408 ± 45 pF) than of the normal myotubes (299 ± 34 pF) of the same apparent size.7. Taken together, these results show that differences in T-and L-type calcium currents between normal and DMD myotubes cannot simply explain all observed alterations in calcium homeostasis in DMD myotubes, thus suggesting that other transmembrane calcium transport mechanisms must also be altered in DMD myotubes compared with normal myotubes.

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“…Moreover, we recorded the resting membrane potential after the depletion protocol in minidysϩ SolD6 myotubes and obtained a mean value of Ϫ61 mV. The depletion protocol leads to low depolarization (around 6 mV depolarization for minidysϩ SolD6 and around 4 mV depolarization for dysϪSolC1), but the membrane potential remains underneath the activation threshold of L-type calcium channels, which is normally around Ϫ30 mV in human (34,35) and rat (36) myotubes and in wild type fibers (37). Nifedipine was used in minidysϩ SolD6 transfected with ␣1-syntrophin siRNA (supplemental Fig.…”

Section: Requirement Of ␣1-syntrophin Ph1a and Pdz Domains (N Terminumentioning

confidence: 99%

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Sabourin

Lamiche

Vandebrouck

et al. 2009

Journal of Biological Chemistry

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The dystrophin-associated protein complex (DAPC) is essential for skeletal muscle, and the lack of dystrophin in Duchenne muscular dystrophy results in a reduction of DAPC components such as syntrophins and in fiber necrosis. By anchoring various molecules, the syntrophins may confer a role in cell signaling to the DAPC. Calcium disorders and abnormally elevated cation influx in dystrophic muscle cells have suggested that the DAPC regulates some sarcolemmal cationic channels. We demonstrated previously that minidystrophin and ␣1-syntrophin restore normal cation entry in dystrophin-deficient myotubes and that sarcolemmal TRPC1 channels associate with dystrophin and the bound PDZ domain of ␣1-syntrophin. This study shows that small interfering RNA (siRNA) silencing of ␣1-syntrophin dysregulated cation influx in myotubes. Moreover, deletion of the PDZcontaining domain prevented restoration of normal cation entry by ␣1-syntrophin transfection in dystrophin-deficient myotubes. TRPC1 and TRPC4 channels are expressed at the sarcolemma of muscle cells; forced expression or siRNA silencing showed that cation influx regulated by ␣1-syntrophin is supported by TRPC1 and TRPC4. A molecular association was found between TRPC1 and TRPC4 channels and the ␣1-syntrophin-dystrophin complex. TRPC1 and TRPC4 channels may form sarcolemmal channels anchored to the DAPC, and ␣1-syntrophin is necessary to maintain the normal regulation of TRPC-supported cation entry in skeletal muscle. Cation channels with DAPC form a signaling complex that modulates cation entry and may be crucial for normal calcium homeostasis in skeletal muscles.

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Calcium currents in normal and dystrophic human skeletal muscle cells in culture

Cited by 25 publications

References 28 publications

Kinetics of inactivation and restoration from inactivation of the L‐type calcium current in human myotubes

Kinetics of inactivation and restoration from inactivation of the L‐type calcium current in human myotubes

Calcium currents and transients in co‐cultured contracting normal and Duchenne muscular dystrophy human myotubes

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

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