Administration of granulocyte colony-stimulating factor facilitates the regenerative process of injured mice skeletal muscle via the activation of Akt/GSK3αβ signals

Naito, Toshihito; Goto, Katsumasa; Morioka, Shigeta; Matsuba, Yusuke; Akema, Tatsuo; Sugiura, T.; Ohira, Yoshinobu; Beppu, Masatoshi; Yoshioka, Toshitada

doi:10.1007/s00421-008-0946-9

Cited by 25 publications

(22 citation statements)

References 39 publications

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“…Eight weeks of G-CSF treatment (30 μg/kg/day) increased Akt phosphorylation in neural tissue of ALS mice (Pitzer et al, 2008). G-CSF also increased Akt phosphorylation in regenerating skeletal muscle after myotoxic injury (Naito et al, 2009). These observations support a role for G-CSF in improving muscle health following injury.…”

Section: Introductionmentioning

confidence: 99%

“…In skeletal muscle, G-CSF treatment improves force recovery, activates satellite cells and increases muscle mass following crush injury (Stratos et al, 2007). G-CSF treatment increases muscle repair following a local cardiotoxin (CTX) injection in mice (Naito et al, 2009) and increases muscle function in mouse models of amyotrophic lateral sclerosis (ALS) (Pitzer et al, 2008). Eight weeks of G-CSF treatment (30 μg/kg/day) increased Akt phosphorylation in neural tissue of ALS mice (Pitzer et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle

et al. 2014

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Granulocyte-colony stimulating factor (G-CSF) increases recovery of rodent skeletal muscles after injury, and increases muscle function in rodent models of neuromuscular disease. However, the mechanisms by which G-CSF mediates these effects are poorly understood. G-CSF acts by binding to the membrane spanning G-CSFR and activating multiple intracellular signaling pathways. Expression of the G-CSFR within the haematopoietic system is well known, but more recently it has been demonstrated to be expressed in other tissues. However, comprehensive characterization of G-CSFR expression in healthy and diseased skeletal muscle, imperative before implementing G-CSF as a therapeutic agent for skeletal muscle conditions, has been lacking. Here we show that the G-CSFR is expressed in proliferating C2C12 myoblasts, differentiated C2C12 myotubes, human primary skeletal muscle cell cultures and in mouse and human skeletal muscle. In mdx mice, a model of human Duchenne muscular dystrophy (DMD), G-CSF mRNA and protein was down-regulated in limb and diaphragm muscle, but circulating G-CSF ligand levels were elevated. G-CSFR mRNA in the muscles of mdx mice was up-regulated however steady-state levels of the protein were down-regulated. We show that G-CSF does not influence C2C12 myoblast proliferation, differentiation or phosphorylation of Akt, STAT3, and Erk1/2. Media change alone was sufficient to elicit increases in Akt, STAT3, and Erk1/2 phosphorylation in C2C12 muscle cells and suggest previous observations showing a G-CSF increase in phosphoprotein signaling be viewed with caution. These results suggest that the actions of G-CSF may require the interaction with other cytokines and growth factors in vivo, however these data provides preliminary evidence supporting the investigation of G-CSF for the management of muscular dystrophy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle

et al. 2014

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“…CSF3R is expressed in regenerating myocytes [11] and enhances proliferation of satellite cells in vivo [11,47]. Administration of G-CSF facilitates the regeneration of cardiotoxin-injured SKM [48] and protects against muscle degeneration in MDX mice [16]. Some progress has also been made in order to investigate whether the effects of G-CSF on muscle cells can be observed in vitro where myoblasts are deprived of their natural niche.…”

Section: Discussionmentioning

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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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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“…Of particular interest is Akt, a kinase known to increase skeletal muscle hypertrophy and attenuate skeletal muscle atrophy in rodents [6,41,37,23,26]. G-CSF treatment increased Akt phosphorylation in regenerating skeletal muscle following myotoxic injury [34]. Whether this influenced protein synthesis or protein degradation was not investigated.…”

Section: Introductionmentioning

confidence: 98%

“…Granulocyte-colony stimulating factor (G-CSF) is a cytokine that is emerging as a potential therapeutic agent to improve muscle repair and restore function following muscle damage [48,34]. Treatment with G-CSF has been shown to increases skeletal muscle force recovery following crush injury in rodents [48].…”

Section: Introductionmentioning

confidence: 99%

G-CSF treatment can attenuate dexamethasone-induced reduction in C2C12 myotube protein synthesis

et al. 2015

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Administration of granulocyte colony-stimulating factor facilitates the regenerative process of injured mice skeletal muscle via the activation of Akt/GSK3αβ signals

Cited by 25 publications

References 39 publications

G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle

G-CSF does not influence C2C12 myogenesis despite receptor expression in healthy and dystrophic skeletal muscle

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

G-CSF treatment can attenuate dexamethasone-induced reduction in C2C12 myotube protein synthesis

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