G-CSF influences mouse skeletal muscle development and regeneration by stimulating myoblast proliferation

Hara, Motoki; Yuasa, Shinsuke; Shimoji, Koki; Onizuka, Takeshi; Hayashiji, Nozomi; Ohno, Yohei; Arai, T.; Hattori, Fumiyuki; Kaneda, Ruri; Kimura, Kensuke; Makino, Shinji; Sano, Motoaki; Fukuda, Keiichi

doi:10.1083/jcb1931oia1

Cited by 21 publications

(36 citation statements)

References 1 publication

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“…On the one hand, it is speculated that G‐CSF acts as a hematopoietic growth factor that stimulates neutrophils and other immune cell types in response to inflammatory signals. On the other hand, animal studies demonstrated a role of G‐CSF in promoting muscle development and regeneration after muscle destruction (Hara et al., ). We did not find a correlation between markers of muscle damage and G‐CSF.…”

Section: Discussionmentioning

confidence: 99%

Progenitor cell mobilization after exercise is related to systemic levels of G‐CSF and muscle damage

Krüger

Pilat

Schild

et al. 2014

Scandinavian Med Sci Sports

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Different types of exercise are characterized by the ability to induce specific physiological stimuli that might be able to induce the mobilization of progenitor cells. The aim of the current study was to investigate the mobilization of hematopoietic progenitor cells (HPCs) and endothelial progenitor cells (EPCs) in response to endurance, resistance, and eccentric endurance exercise and their relation to markers of muscle damage and inflammation. Healthy male subjects performed acute bouts of either endurance exercise, resistance exercise, or eccentric endurance exercise. Numbers of progenitor cells and several markers of muscle damage and inflammation were determined. Although the endurance exercise was followed by an immediate and short increase of both HPCs and EPCs, the eccentric exercise evoked a long lasting increase up to 24 h for HPCs and 48 h for EPCs (P < 0.05). After resistance exercise, an increase of HPCs was only found 3 h after exercise (P < 0.05). A correlation was found between mobilized progenitor cells and systemic levels of granulocyte colony-stimulating factor (G-CSF) levels (r = 0.54 and r = 0.51, P < 0.05) as well as for HPCs and creatine kinase levels (r = 0.57, P < 0.05). These results suggest that mobilization of progenitor cells is related to the type of exercise and possibly mediated by G-CSF and muscle damage.

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Section: Discussionmentioning

confidence: 99%

Progenitor cell mobilization after exercise is related to systemic levels of G‐CSF and muscle damage

Krüger

Pilat

Schild

et al. 2014

Scandinavian Med Sci Sports

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show abstract

“…Some data document that G‐CSF does not influence myoblasts proliferation or differentiation in vitro . Other lines of evidence imply that G‐CSF receptor is expressed in C2C12 myoblasts, and that G‐CSF strongly induces myoblasts proliferation in vitro . Moreover, the expression of G‐CSF receptor was shown to be elevated in regenerating muscle in mice, starting from day 3 to 8 after ctx injury, that is, at the stages when myoblasts proliferate .…”

Section: Discussionmentioning

confidence: 99%

Stromal derived factor‐1 and granulocyte‐colony stimulating factor treatment improves regeneration of Pax7−/− mice skeletal muscles

Kowalski

Archacki

Archacka

et al. 2015

J cachexia sarcopenia muscle

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BackgroundThe skeletal muscle has the ability to regenerate after injury. This process is mediated mainly by the muscle specific stem cells, that is, satellite cells. In case of extensive damage or under pathological conditions, such as muscular dystrophy, the process of muscle reconstruction does not occur properly. The aim of our study was to test whether mobilized stem cells, other than satellite cells, could participate in skeletal muscle reconstruction.MethodsExperiments were performed on wild‐type mice and mice lacking the functional Pax7 gene, that is, characterized by the very limited satellite cell population. Gastrocnemius mice muscles were injured by cardiotoxin injection, and then the animals were treated by stromal derived factor‐1 (Sdf‐1) with or without granulocyte‐colony stimulating factor (G‐CSF) for 4 days. The muscles were subjected to thorough assessment of the tissue regeneration process using histological and in vitro methods, as well as evaluation of myogenic factors' expression at the transcript and protein levels.ResultsStromal derived factor‐1 alone and Sdf‐1 in combination with G‐CSF significantly improved the regeneration of Pax7−/− skeletal muscles. The Sdf‐1 and G‐CSF treatment caused an increase in the number of mononucleated cells associated with muscle fibres. Further analysis showed that Sdf‐1 and G‐CSF treatment led to the rise in the number of CD34+ and Cxcr4+ cells and expression of Cxcr7.ConclusionsStromal derived factor‐1 and G‐CSF stimulated regeneration of the skeletal muscles deficient in satellite cells. We suggest that mobilized CD34+, Cxcr4+, and Cxcr7+ cells can efficiently participate in the skeletal muscle reconstruction and compensate for the lack of satellite cells.

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“…Interestingly, a recent study from Hara et al . showed that compared with control mice, CSF3R knockout mice had smaller diameter of rectus femoris muscle and body size. In addition, skeletal muscle regeneration was impaired in the adult CSF3R knockout mice .…”

Section: Skeletal Muscle Resident Macrophage Ontogeny and Homeostasismentioning

confidence: 96%

“… showed that compared with control mice, CSF3R knockout mice had smaller diameter of rectus femoris muscle and body size. In addition, skeletal muscle regeneration was impaired in the adult CSF3R knockout mice . These findings suggest that skeletal muscle resident macrophages development might not be through CSF1, but by other cytokines (e.g., IL‐34), as observed in microglia and Langerhans cells.…”

Section: Skeletal Muscle Resident Macrophage Ontogeny and Homeostasismentioning

confidence: 96%

Chronic inflammation in skeletal muscle impairs satellite cells function during regeneration: can physical exercise restore the satellite cell niche?

et al. 2018

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Chronic inflammation impairs skeletal muscle regeneration. Although many cells are involved in chronic inflammation, macrophages seem to play an important role in impaired muscle regeneration since these cells are associated with skeletal muscle stem cell (namely, satellite cells) activation and fibro-adipogenic progenitor cell (FAP) survival. Specifically, an imbalance of M1 and M2 macrophages seems to lead to impaired satellite cell activation, and these are the main cells that function during skeletal muscle regeneration, after muscle damage. Additionally, this imbalance leads to the accumulation of FAPs in skeletal muscle, with aberrant production of pro-fibrotic factors (e.g., extracellular matrix components), impairing the niche for proper satellite cell activation and differentiation. Treatments aiming to block the inflammatory pro-fibrotic response are partially effective due to their side effects. Therefore, strategies reverting chronic inflammation into a pro-regenerative pattern are required. In this review, we first describe skeletal muscle resident macrophage ontogeny and homeostasis, and explain how macrophages are replenished after muscle injury. We next discuss the potential role of chronic physical activity and exercise in restoring the M1 and M2 macrophage balance and consequently, the satellite cell niche to improve skeletal muscle regeneration after injury.

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G-CSF influences mouse skeletal muscle development and regeneration by stimulating myoblast proliferation

Cited by 21 publications

References 1 publication

Progenitor cell mobilization after exercise is related to systemic levels of G‐CSF and muscle damage

Progenitor cell mobilization after exercise is related to systemic levels of G‐CSF and muscle damage

Stromal derived factor‐1 and granulocyte‐colony stimulating factor treatment improves regeneration of Pax7−/− mice skeletal muscles

Chronic inflammation in skeletal muscle impairs satellite cells function during regeneration: can physical exercise restore the satellite cell niche?

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