Effects of Interleukin-6, Leukemia Inhibitory Factor, and Ciliary Neurotrophic Factor on the Proliferation and Differentiation of Adult Human Myoblasts

Wang, Xuan; Wu, Haitao; Zhang, Zhenxing; Liu, Shuhong; Yang, Jian; Chen, Xiaoping; Fan, Ming; Wang, Xiaomin

doi:10.1007/s10571-007-9247-9

Cited by 45 publications

(38 citation statements)

References 31 publications

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“…For example, application of IL-6 to myoblasts in culture increases their proliferation but not cell fusion (125). NF-B induction of IL-6 expression can also have profound effects on muscle differentiation and play functionally important roles in muscle growth by acting on later stages of the differentiation process.…”

Section: Do Neutrophil-derived or M1 Macrophage-derived Molecules Modmentioning

confidence: 99%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

894

987

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Tidball JG, Villalta SA. Regulatory interactions between muscle and the immune system during muscle regeneration. Am J Physiol Regul Integr Comp Physiol 298: R1173-R1187, 2010. First published March 10, 2010 doi:10.1152/ajpregu.00735.2009.-Recent discoveries reveal complex interactions between skeletal muscle and the immune system that regulate muscle regeneration. In this review, we evaluate evidence that indicates that the response of myeloid cells to muscle injury promotes muscle regeneration and growth. Acute perturbations of muscle activate a sequence of interactions between muscle and inflammatory cells. The initial inflammatory response is a characteristic Th1 inflammatory response, first dominated by neutrophils and subsequently by CD68 ϩ M1 macrophages. M1 macrophages can propagate the Th1 response by releasing proinflammatory cytokines and cause further tissue damage through the release of nitric oxide. Myeloid cells in the early Th1 response stimulate the proliferative phase of myogenesis through mechanisms mediated by TNF-␣ and IL-6; experimental prolongation of their presence is associated with delayed transition to the early differentiation stage of myogenesis. Subsequent invasion by CD163ϩ /CD206 ϩ M2 macrophages attenuates M1 populations through the release of anti-inflammatory cytokines, including IL-10. M2 macrophages play a major role in promoting growth and regeneration; their absence greatly slows muscle growth following injury or modified use and inhibits muscle differentiation and regeneration. Chronic muscle injury leads to profiles of macrophage invasion and function that differ from acute injuries. For example, mdx muscular dystrophy yields invasion of muscle by M1 macrophages, but their early invasion is accompanied by a subpopulation of M2a macrophages. M2a macrophages are IL-4 receptor ϩ /CD206 ϩ cells that reduce cytotoxicity of M1 macrophages. Subsequent invasion of dystrophic muscle by M2c macrophages is associated with progression of the regenerative phase in pathophysiology. Together, these findings show that transitions in macrophage phenotype are an essential component of muscle regeneration in vivo following acute or chronic muscle damage. skeletal muscle; macrophage; neutrophil; muscular dystrophy; chemokines SKELETAL MUSCLE HAS A REMARKABLE capacity for repair, even following severe damage. Experimental findings show that crushing muscle, killing muscle by the injection of toxins, mechanical destruction caused by large, lengthening stretches, or killing muscle fibers by freezing can be followed by the successful regeneration of muscle that leads to recovery of normal structure and function. The regenerative capacity of skeletal muscle relies largely on the presence of a population of mononucleated, myogenic cells, called satellite cells, that retain their ability to proliferate and then differentiate to either fuse with existing fibers or with other myogenic cells to generate new fibers. Thus, perturbations to the processes that normally regulate the activation, proliferat...

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Section: Do Neutrophil-derived or M1 Macrophage-derived Molecules Modmentioning

confidence: 99%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

894

987

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“…5B), indicating that the proliferation of myoblast was impaired in IL-6 Ϫ/Ϫ mice. It has been reported that exogenous IL-6 could promote the proliferation of myoblast (13,28), and we determined a dose response effect of IL-6. The recombinant IL-6 was added to the culture of C2C12 myoblasts with different concentrations, recombinant IL-6 could promote the proliferation of myoblast, especially at the concentration of 10 ng/ml (the percentage of BrdU-positive cells in control group was ϳ15% and in that group, 10 ng/ml IL-6 was ϳ35%) (Fig.…”

Section: Il-6mentioning

confidence: 99%

“…Previous studies have demonstrated that exogenous IL-6 could promote the proliferation of human and mouse myoblast cultured in vitro and in vitro (13,28). Serrano et al reported that IL-6 can be produced by myoblasts and promoted myoblast proliferation and hypertrophy intrinsically (14); therefore, there is a possibility of that abnormal myoblasts in IL-6 Ϫ/Ϫ mice may also contribute to impaired muscle regeneration.…”

Section: Cd11bmentioning

confidence: 99%

“…Exogenous recombination IL-6 influence the proliferation and differentiation of cultured myoblast derived from human or mouse muscle. Its functions were performed mainly via the activation of STAT3 signaling pathway (13)(14)(15). Additionally, the cytokine IL-6 is also secreted by T cells, fibro-blasts, and other cells, classically associated with the control of immune responses to trauma or other tissue damage.…”

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confidence: 99%

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Interleukin-6/Signal Transducer and Activator of Transcription 3 (STAT3) Pathway Is Essential for Macrophage Infiltration and Myoblast Proliferation during Muscle Regeneration

Zhang

et al. 2013

Journal of Biological Chemistry

243

202

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Background: Interleukin-6 (IL-6), as a multifunctional cytokine, was involved in the inflammation microenvironment of muscle regeneration. Results: In mice lacking IL-6, less macrophage recruitment and decreased myoblast proliferation impairs muscle regeneration. Conclusion: In monocytes/macrophages, activation of the IL-6/STAT3 pathway is critical to macrophage migration and myoblast proliferation during muscle regeneration. Significance: IL-6/STAT3 pathway is essential for muscle regeneration.

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“…These results suggest that expression of IL-6 in stimulated skeletal muscle cells is mediated by extracellular ATP and nucleotide receptors, involving IP 3-dependent calcium signals as an early step that triggers a positive IL-6 autocrine loop. myokines; muscle plasticity; exercise; signal transducer and activator of transcription 3; purinergic signaling (IL-6) is a proinflammatory cytokine that has been related to several processes in skeletal muscle cells, including in vitro proliferation and differentiation, regeneration of damaged adult fibers, atrophy, and hypertrophy, among others (7,35,71,86). Variations of IL-6 expression levels have been related to metabolic changes in skeletal muscle undergoing different exercise protocols (17,66,77).…”

mentioning

confidence: 99%

Electrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca²⁺signals and an IL-6 autocrine loop

Bustamante

Fernández‐Verdejo

Jaimovich

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Bustamante M, Fernández-Verdejo R, Jaimovich E, Buvinic S. Electrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca 2ϩ signals and an IL-6 autocrine loop. Am J Physiol Endocrinol Metab 306: E869 -E882, 2014. First published February 11, 2014 doi:10.1152/ajpendo.00450.2013 is an important myokine that is highly expressed in skeletal muscle cells upon exercise. We assessed IL-6 expression in response to electrical stimulation (ES) or extracellular ATP as a known mediator of the excitation-transcription mechanism in skeletal muscle. We examined whether the canonical signaling cascade downstream of IL-6 (IL-6/JAK2/STAT3) also responds to muscle cell excitation, concluding that IL-6 influences its own expression through a positive loop. Either ES or exogenous ATP (100 M) increased both IL-6 expression and p-STAT3 levels in rat myotubes, a process inhibited by 100 M suramin and 2 U/ml apyrase. ATP also evoked IL-6 expression in both isolated skeletal fibers and extracts derived from whole FDB muscles. ATP increased IL-6 release up to 10-fold. STAT3 activation evoked by ATP was abolished by the JAK2 inhibitor HBC. Blockade of secreted IL-6 with a neutralizing antibody or preincubation with the STAT3 inhibitor VIII reduced STAT3 activation evoked by extracellular ATP by 70%. Inhibitor VIII also reduced by 70% IL-6 expression evoked by ATP, suggesting a positive IL-6 loop. In addition, ATP increased up to 60% the protein levels of SOCS3, a negative regulator of the IL-6 signaling pathway. On the other hand, intracellular calcium chelation or blockade of IP 3-dependent calcium signals abolished STAT3 phosphorylation evoked by either extracellular ATP or ES. These results suggest that expression of IL-6 in stimulated skeletal muscle cells is mediated by extracellular ATP and nucleotide receptors, involving IP 3-dependent calcium signals as an early step that triggers a positive IL-6 autocrine loop.

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Effects of Interleukin-6, Leukemia Inhibitory Factor, and Ciliary Neurotrophic Factor on the Proliferation and Differentiation of Adult Human Myoblasts

Cited by 45 publications

References 31 publications

Regulatory interactions between muscle and the immune system during muscle regeneration

Regulatory interactions between muscle and the immune system during muscle regeneration

Interleukin-6/Signal Transducer and Activator of Transcription 3 (STAT3) Pathway Is Essential for Macrophage Infiltration and Myoblast Proliferation during Muscle Regeneration

Electrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca²⁺signals and an IL-6 autocrine loop

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Effects of Interleukin-6, Leukemia Inhibitory Factor, and Ciliary Neurotrophic Factor on the Proliferation and Differentiation of Adult Human Myoblasts

Cited by 45 publications

References 31 publications

Regulatory interactions between muscle and the immune system during muscle regeneration

Regulatory interactions between muscle and the immune system during muscle regeneration

Interleukin-6/Signal Transducer and Activator of Transcription 3 (STAT3) Pathway Is Essential for Macrophage Infiltration and Myoblast Proliferation during Muscle Regeneration

Electrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca2+signals and an IL-6 autocrine loop

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Electrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca²⁺signals and an IL-6 autocrine loop