Determination of depolarisation- and agonist-evoked calcium fluxes on skeletal muscle cells in primary culture

Szappanos, Henrietta Cserné; Cseri, J.; Deli, Tamás; Kovács, László; Csernoch, László

doi:10.1016/j.jbbm.2003.12.002

Cited by 19 publications

(20 citation statements)

References 33 publications

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“…4A) on control, T95-myotubes, or on T51-myotubes by changing to 140 mM KCl. It resulted, as expected (27)(28)(29), in an increase in intracellular calcium concentration followed by a return to the basal level in control myotubes as well as in T51-myotubes. Nevertheless, in T95-myotubes, this effect was almost abolished, and depolarization induced only a minor calcium release (Fig.…”

Section: Trisk 95 or Trisk 51 Overexpression Does Not Modify Expressisupporting

confidence: 75%

Triadin (Trisk 95) Overexpression Blocks Excitation-Contraction Coupling in Rat Skeletal Myotubes

Rezgui

Vassilopoulos

Brocard

et al. 2005

Journal of Biological Chemistry

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To identify the function of triadin in skeletal muscle, adenovirusmediated overexpression of Trisk 95 or Trisk 51, the two major skeletal muscle isoforms, was induced in rat skeletal muscle primary cultures, and the physiological behavior of the modified cells was analyzed. Overexpression did not modify the expression level of their protein partners ryanodine receptor, dihydropyridine receptor, and the other triadin. Caffeine-induced calcium release was also unaffected by triadin overexpression. Nevertheless, in the absence of extracellular calcium, depolarization-induced calcium release was almost abolished in Trisk 95 overexpressing myotubes (T95 myotubes), and not modified in Trisk 51 overexpressing myotubes (T51 myotubes). This was not because of a modification of dihydropyridine receptors, as depolarization in presence of external calcium still induced a calcium release, and the activation curve of dihydropyridine receptor was unchanged, in both T95 and T51 myotubes. The calcium release complex was also maintained in T95 myotubes as Trisk 95, ryanodine receptor, dihydropyridine receptor, and Trisk 51 were still co-localized. The effect of Trisk 95 overexpression on depolarization-induced calcium release was reversed by a simultaneous infection with an antisense Trisk 95 adenovirus, indicating the specificity of this effect. Thus, the level of Trisk 95 and not Trisk 51 is important on regulating the calcium release complex, and an excess of this protein can lead to an inhibition of the physiological function of the complex. In skeletal muscle cells, excitation-contraction (E-C)2 coupling is the process by which depolarization of the plasma membrane produces a large transient release of Ca 2ϩ from the sarcoplasmic reticulum, which in turn triggers contraction. Dihydropyridine receptors (DHPRs), the L-type Ca 2ϩ channels localized in the T-tubule membrane, serve as the voltage sensors for E-C coupling (1, 2) and activate ryanodine receptors (RyRs), the intracellular Ca 2ϩ release channels of the sarcoplasmic reticulum membrane (3, 4). In skeletal muscle, entry of Ca 2ϩ through DHPR is not required for E-C coupling (5). Instead, a voltage-dependent conformational change in the II-III loop of the skeletal muscle DHPR ␣1 subunit (Cav1.1) activates the skeletal muscle ryanodine receptor, RyR1. Activation of RyR1 results in a release of Ca 2ϩ from the sarcoplasmic reticulum intracellular stores into the cytosol, which in turn activates the cellular contractile apparatus to initiate muscle contraction. In cardiac muscle, the entry of external calcium through DHPR is required to induce activation of RyR and release of internal Ca 2ϩ via RyR, a mechanism known as calcium-induced calcium release. Calcium-induced calcium release is not the initial mechanism responsible of Ca 2ϩ release in skeletal muscle, but it can contribute to the amplification of the signal, and both calcium-induced calcium release and conformational coupling are involved in skeletal muscle contraction, to different extents (6).Triadin is a transmem...

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Section: Trisk 95 or Trisk 51 Overexpression Does Not Modify Expressisupporting

confidence: 75%

Triadin (Trisk 95) Overexpression Blocks Excitation-Contraction Coupling in Rat Skeletal Myotubes

Rezgui

Vassilopoulos

Brocard

et al. 2005

Journal of Biological Chemistry

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“…The isolation of adult skeletal muscle fibers followed a protocol described previously (Szappanos et al 2004). In brief, muscle fibers were separated by 90 min enzymatic digestion at 37°C in a shaker water bath with type 2 collagenase (Sigma) containing solution.…”

Section: Measurement Of Resting Calcium Levelsmentioning

confidence: 99%

Fluvastatin-induced alterations of skeletal muscle function in hypercholesterolaemic rats

Füzi

Palicz

Vincze

et al. 2011

J Muscle Res Cell Motil

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Although statins, the most widely used drugs in the treatment of hyperlipidaemia, are generally accepted as efficient and safe drugs their side-effects on skeletal muscle have been reported with increasing frequency in the past years. The lack of an appropriate animal model in which these side effects would consistently be observed is one of the most important drawbacks in studying statin associated myopathy. To overcome this and enable the studying of the effects of fluvastatin on skeletal muscles an animal model with high blood cholesterol levels was developed. In these animals cholesterol levels rose more than seven fold (from soleus the duration of twitch and tetanic force was shortened. These results clearly indicate that statin administration in these animals results in a myopathy characterized by decreased muscle force and elevated plasma creatine kinase level.

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“…31 Briefly, cells were incubated for 90 min at 37°C with 15 lM fura-2 AM (Molecular Probes, Eugene, OR) in the presence of 150 nM neostigmine (Pharmamagist, Budapest, Hungary) and 0.02% pluronic (Sigma). Coverslips were then washed with normal HEPES Tyrode's solution (137 mM NaCl, 5.4 mM KCl, 0.5 mM MgCl 2 , 1.8 mM CaCl 2 , 11.8 mM HEPESNaOH, 1 g/l glucose, pH 7.4).…”

Section: Fluorescent Measurement Of [Camentioning

confidence: 99%

Functional genomics of calcium channels in human melanoma cells

Deli

Varga

Ádám

et al. 2007

Intl Journal of Cancer

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Ca2+‐signaling of human melanoma is in the focus of intensive research since the identification of the role of WNT‐signaling in melanomagenesis. Genomic and functional studies pointed to the important role of various Ca2+ channels in melanoma, but these data were contradictory. In the present study we clearly demonstrate, in a number of different ways including microarray analysis, DNA sequencing and immunocytochemistry, that various human melanoma cell lines and melanoma tissues overexpress ryanodine receptor type 2 (RyR2) and express P2X7 channel proteins as compared to melanocytes. These channels, although retain some of their usual characteristics and pharmacological properties, display unique features in melanoma cells, including a functional interaction between the two molecules. Unlike P2X7, RyR2 does not function as a calcium channel. On the other hand, the P2X7 receptor has an antiapoptotic function in melanoma cells, since ATP‐activation suppresses induced apoptosis, while knock down of the gene expression significantly enhances that. © 2007 Wiley‐Liss, Inc.

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Determination of depolarisation- and agonist-evoked calcium fluxes on skeletal muscle cells in primary culture

Cited by 19 publications

References 33 publications

Triadin (Trisk 95) Overexpression Blocks Excitation-Contraction Coupling in Rat Skeletal Myotubes

Triadin (Trisk 95) Overexpression Blocks Excitation-Contraction Coupling in Rat Skeletal Myotubes

Fluvastatin-induced alterations of skeletal muscle function in hypercholesterolaemic rats

Functional genomics of calcium channels in human melanoma cells

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