Oxidative stress in skeletal muscle stimulates early expression of Rad in a mouse model of amyotrophic lateral sclerosis

Halter, Benoît; Aguilar, José-Luis González de; Frydman, René; Petri, Susanne; Fricker, Bastien; Echaniz‐Laguna, Andoni; Dupuis, Luc; Larmet, Yves; Loeffler, Jean‐Philippe

doi:10.1016/j.freeradbiomed.2010.01.014

Cited by 58 publications

(63 citation statements)

References 53 publications

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“…To assess the effect of PEGF on the RNA markers of NMJ disintegration, shown previously to be altered in mutant SOD1 mice and in some patients [26,37], we quantified transcripts of cholinergic receptor, nicotinic, alpha 1 (Chrna1) and Ras-related associated with diabetes (Rrad) at the symptomatic age of 15 weeks. As denervation of SKM fibers proceeds, they become hypersensitive to electrical stimulation due to stimulated expression of cholinergic receptors, including Chrna1, that are under transcriptional control of myogenic regulatory factors [38,39,40].…”

Section: Resultsmentioning

confidence: 99%

“…Like that of Chrna1 , the expression of Rrad is progressively upregulated towards the more severe denervation pathology in SOD1-G93A mice [25,26,37]. Unlike that of Chrna1 , however, Rrad upregulation seems to primarily rely on increased reactive oxygen species as its induction can be antagonized by antioxidant treatment [37]. Here, as expected, Chrna1 and Rrad were found to be extremely upregulated in SOD1-G93A mice compared to their wild-type littermates (fig.…”

Section: Resultsmentioning

confidence: 99%

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Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro

Rando¹,

Gasco²,

Torre³

et al. 2016

Neurodegener Dis

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Background: Amyotrophic lateral sclerosis (ALS) causes loss of upper and lower motor neurons as well as skeletal muscle (SKM) dysfunction and atrophy. SKM is one of the tissues involved in the development of ALS pathology, and studies in a SOD1-G93A mouse model of ALS have demonstrated alterations in SKM degeneration/regeneration marker expression in vivo and defective mutant myoblast proliferation in vitro. Granulocyte colony-stimulating factor (G-CSF) has been shown to alleviate SOD1-G93A pathology. However, it is unknown whether G-CSF may have a direct effect on SKM or derived myoblasts. Objective: To investigate effects of G-CSF and its analog pegfilgrastim (PEGF) on SOD1-G93A- associated SKM markers in vivo and those of G-CSF on myoblast proliferation in vitro. Methods: The effect of PEGF treatment on hematopoietic stem cell mobilization, survival, and motor function was determined. RNA expression of SKM markers associated with mutant SOD1 expression was quantified in response to PEGF treatment in vivo, and the effect of G-CSF on the proliferation of myoblasts derived from mutant and control muscles was determined in vitro. Results: Positive effects of PEGF on hematopoietic stem cell mobilization, survival, and functional assays in SOD1-G93A animals were confirmed. In vivo PEGF treatment augmented the expression of its receptor Csf3r and alleviated typical markers for mutant SOD1 muscle. Additionally, G-CSF was found to directly increase the proliferation of SOD1-G93A, but not wild-type primary myoblasts in vitro. Conclusion: Our results support the beneficial role of the G-CSF analog PEGF in a SOD1-G93A model of ALS. Thus, G-CSF andits analogs may be directly beneficial in diseases where the SKM function is compromised.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro

Rando¹,

Gasco²,

Torre³

et al. 2016

Neurodegener Dis

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“…25 By the same token, one may speculate that pathological increases in RGK protein expression may have similar atrophic effects in a broad spectrum of disorders that affect skeletal muscle. In particular, Rad expression is substantially enhanced in muscle obtained from type II diabetics, 14,16 amyotrophic lateral sclerosis patients, 18,26 dystrophic (mdx) mice 17 and dennervated Table 1. Throughout, error bars represent ± seM.…”

Section: Discussionmentioning

confidence: 99%

“…18 Thus, the potential role for RGK proteins as agents of pathological muscle atrophy highlights the importance of understanding the mechanisms that these small GTP-binding proteins employ to regulate L-type channel activity in skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

“…As a means to investigate the effects of the RGK proteins thought to be endogenously expressed in skeletal muscle (i.e., Rad, Gem and Rem) [14][15][16][17][18] on the known functions of Ca V 1.1, we overexpressed one of these muscle RGK protein isoforms in cultured "normal" myotubes and confirmed expression via a fused Venus fluorescent protein tag. When viewed with confocal microscopy, V-Rad, V-Gem and V-Rem each displayed a diffuse fluorescence distribution similar to that of unfused YFP (Fig.…”

Section: Rgk Proteins Alter Myotube Morphology and Inhibit Ec Couplingmentioning

confidence: 99%

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RGK protein-mediated impairment of slow depolarization- dependent Ca²⁺entry into developing myotubes

et al. 2014

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Moringa oleifera Lam.ameliorates the muscles function recovery following an induced insult to the Sciatic nerve in a mouse model

Razzaq

Malik

Saeed

et al. 2020

Food Science & Nutrition

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Peripheral nerve injury (PNI) is an incapacitating situation and has no effective therapy until now. We examined the possible role of crude leaves of Moringa oleifera Lam. at 200 mg/kg body weight in accelerating the functional regain in the sciatic nerve lesion induced mouse model (Adult male albino mice (BALB/c). Motor functions were evaluated by using the sciatic functional index, muscle mass, and muscle grip strength measurement, whereas the sensory functions were evaluated by using the hot plate test. Blood glucose levels and blood cell composition were also analyzed. We found that the Moringa oleifera crude leaves endorse the sensory and motor functions reclamation following the PNI with a statistically significant difference (p < .05). It also revitalizes the gastrocnemius muscle by mass restoration with glycemic management perspective. Conclusively, the crude powder of Moringa oleifera leaves exhibited a function restoration boosting property and further detailed studies for its application as a therapeutic agent are strongly recommended.

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Oxidative stress in skeletal muscle stimulates early expression of Rad in a mouse model of amyotrophic lateral sclerosis

Cited by 58 publications

References 53 publications

Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro

Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro

RGK protein-mediated impairment of slow depolarization- dependent Ca²⁺entry into developing myotubes

Moringa oleifera Lam.ameliorates the muscles function recovery following an induced insult to the Sciatic nerve in a mouse model

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Oxidative stress in skeletal muscle stimulates early expression of Rad in a mouse model of amyotrophic lateral sclerosis

Cited by 58 publications

References 53 publications

Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro

Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro

RGK protein-mediated impairment of slow depolarization- dependent Ca2+entry into developing myotubes

Moringa oleifera Lam.ameliorates the muscles function recovery following an induced insult to the Sciatic nerve in a mouse model

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RGK protein-mediated impairment of slow depolarization- dependent Ca²⁺entry into developing myotubes