Creatine supplementation improves intracellular Ca<sup>2+</sup> handling and survival in <i>mdx</i> skeletal muscle cells

Pulido, Silvia; Passaquin, Anne-Catherine; Leijendekker, W. J.; Challet, Corinne; Wallimann, Theo; Rüegg, Urs T.

doi:10.1016/s0014-5793(98)01399-4

Cited by 116 publications

(84 citation statements)

References 40 publications

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“…However, boys with DMD do not typically present until their preschool years, at which point muscle remodeling has already begun. Consequently, the magnitude of benefit observed from therapies in the mdx model 36,37 might not readily translate to boys with DMD. It is important to note that CrM, which was not robustly beneficial in the current study, has already demonstrated efficacy in boys with DMD when given well after the onset of weakness, 47,52 as well as in mdx mice aged 100 -110 days.…”

Section: Discussionmentioning

confidence: 99%

“…25,47,52 It enhances survival and reduces intracellular calcium accumulation in cultured mdx myoblasts and in primary cell cultures from patients with DMD. 37 CrM-supplemented mdx mice demonstrated reduced necrosis in type II muscle fibers and an enhanced skeletal muscle oxidative capacity. 36 CrM supplementation also increases measures of strength and reduce a marker of bone breakdown in boys with DMD.…”

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confidence: 87%

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Nutritional therapy improves function and complements corticosteroid intervention in mdx mice

et al. 2005

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Corticosteroid therapy for Duchenne muscular dystrophy is effective but associated with long-term side effects. To determine the potential therapeutic benefit from four nutritional compounds (creatine monohydrate, conjugated linoleic acid, ␣-lipoic acid, and ␤-hydroxy-␤-methylbutyrate) alone, in combination, and with corticosteroids (prednisolone), we evaluated the effects on several variables in exercising mdx mice. Outcome measures included grip strength, rotarod performance, serum creatine kinase levels, muscle metabolites, internalized myonuclei, and retroperitoneal fat pad weight. In isolation, each nutritional treatment showed some benefit, with the combination therapy showing the most consistent benefits. Prednisolone and the combination therapy together provided the most consistent evidence of efficacy; increased peak grip strength (P Ͻ 0.05), decreased grip strength fatigue (P Ͻ 0.05), decreased number of internalized myonuclei (P Ͻ 0.01), and smaller retroperitoneal fat pad stores (P Ͻ 0.001). This study provided evidence for therapeutic benefit from a four-compound combination therapy alone, and in conjunction with corticosteroids in the mdx model of DMD.

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Section: Discussionmentioning

confidence: 99%

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confidence: 87%

Nutritional therapy improves function and complements corticosteroid intervention in mdx mice

et al. 2005

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“…Similarly, creatine and in some cases the related analog cyclocreatine (CyCr) exert protective effects in several animal models of neurodegenerative diseases, like Huntington's disease (11), amyotrophic lateral sclerosis (12), and a form of Parkinsonism (13). Likewise, Cr pretreatment of cultured myotubes from dystrophic mdx mice enhanced myotube formation and survival (14). Recent data indicate that Cr reduces muscle necrosis and protects mitochondrial function in vivo in mdx mice (15).…”

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confidence: 97%

Inhibition of the Mitochondrial Permeability Transition by Creatine Kinase Substrates

Dolder

Walzel²,

Speer

et al. 2003

Journal of Biological Chemistry

198

120

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Mitochondria from transgenic mice, expressing enzymatically active mitochondrial creatine kinase in liver, were analyzed for opening of the permeability transition pore in the absence and presence of creatine kinase substrates but with no external adenine nucleotides added. In mitochondria from these transgenic mice, cyclosporin A-inhibited pore opening was delayed by creatine or cyclocreatine but not by ␤-guanidinopropionic acid. This observation correlated with the ability of these substrates to stimulate state 3 respiration in the presence of extramitochondrial ATP. The dependence of transition pore opening on calcium and magnesium concentration was studied in the presence and absence of creatine. If mitochondrial creatine kinase activity decreased (i.e. by omitting magnesium from the medium), protection of permeability transition pore opening by creatine or cyclocreatine was no longer seen. Likewise, when creatine kinase was added externally to liver mitochondria from wild-type mice that do not express mitochondrial creatine kinase in liver, no protective effect on pore opening by creatine and its analog was observed. All these findings indicate that mitochondrial creatine kinase activity located within the intermembrane and intercristae space, in conjunction with its tight functional coupling to oxidative phosphorylation, via the adenine nucleotide translocase, can modulate mitochondrial permeability transition in the presence of creatine. These results are of relevance for the design of creatine analogs for cell protection as potential adjuvant therapeutic tools against neurodegenerative diseases.

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“…13 However, there have been no studies to date that have measured the potential effects on EC coupling, even though this process is critical to force development under both physiologic and pathologic conditions. Therefore we have investigated the potential effects of Cr supplementation on EC coupling, using myotubes from a C2C12 cell line.…”

Section: Dovepressmentioning

confidence: 99%

Creatine supplementation upregulates excitation-contraction coupling in C2C12 myotubes

Calderón-Rivera¹,

Vega²,

Ávila

2010

JRLCR

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Abstract:The main goal of this work was to investigate whether creatine (Cr) might be able to regulate skeletal muscle excitation-contraction (EC) coupling. Myotubes from a C2C12 cell line were exposed to Cr (25 mM, 2-4 hours). Subsequently, the activity of L-type Ca 2+ channels and voltage-gated Ca 2+ release (VGCR) were investigated using the whole-cell patch-clamp technique.Cr upregulated VGCR by 2. -ATPase. We also investigated possible long-term regulation of L-type Ca 2+ channels by Cr. However, chronic treatment with Cr (2-4 days) affected neither the density of I CaL nor the corresponding voltagedependence of activation. The later result was obtained in the face of a 1.7-fold stimulation of myogenesis. Therefore, it cannot be explained by possible desensitization of Cr metabolism. These data could suggest that the functional expression of L-type Ca 2+ channels is not affected by prior acute stimulation of VGCR. Previous work has shown that Cr supplementation enhances muscle strength. Thus, it will be interesting to investigate whether this effect can be at least partially explained by acute stimulation of VGCR.

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Creatine supplementation improves intracellular Ca²⁺ handling and survival in mdx skeletal muscle cells

Cited by 116 publications

References 40 publications

Nutritional therapy improves function and complements corticosteroid intervention in mdx mice

Nutritional therapy improves function and complements corticosteroid intervention in mdx mice

Inhibition of the Mitochondrial Permeability Transition by Creatine Kinase Substrates

Creatine supplementation upregulates excitation-contraction coupling in C2C12 myotubes

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Creatine supplementation improves intracellular Ca2+ handling and survival in mdx skeletal muscle cells

Cited by 116 publications

References 40 publications

Nutritional therapy improves function and complements corticosteroid intervention in mdx mice

Nutritional therapy improves function and complements corticosteroid intervention in mdx mice

Inhibition of the Mitochondrial Permeability Transition by Creatine Kinase Substrates

Creatine supplementation upregulates excitation-contraction coupling in C2C12 myotubes

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Creatine supplementation improves intracellular Ca²⁺ handling and survival in mdx skeletal muscle cells