Effects of leukaemia inhibitory factor and other cytokines on murine and human myoblast proliferation

Austin, L.; Bower, J.; Kurek, JB; Vakakis, N.

doi:10.1016/0022-510x(92)90149-f

Cited by 113 publications

(77 citation statements)

References 8 publications

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“…However, both mRNAs were apparently downregulated in the newly formed myotubes. There are many data showing that LIF is upregulated in regenerating myofibers and that this contributes to the proliferation of myoblasts in vitro (Austin et al 1992;Barnard et al 1994;Bower et al 1995;Kami and Senba 1998). The complex of gp130 and LIFR is also utilized as a signal transducer to mediate the biological actions of CNTF, OM, and CT-1 (Kishimoto et al 1994), but there are no reports suggesting the synthesis of these cytokines in regenerating muscles or their roles in myogenesis in vivo or in vitro.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression of Receptors for IL-6, LIF, and CNTF in Regenerating Skeletal Muscles

Kami

Morikawa²,

Sekimoto³

et al. 2000

J Histochem Cytochem.

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The biological actions of interleukin-6 (IL-6), leukemia inhibitory factor (LIF), and ciliary neurotrophic factor (CNTF) are mediated via respective functional receptor complexes consisting of a common signal-transducing component, gp130, and other specific receptor components, IL-6 receptor α (IL-6R), LIF receptor β (LIFR), and CNTF receptor α (CNTFR). IL-6, LIF, and CNTF are implicated in skeletal muscle regeneration. However, the cell populations that express these receptor components in regenerating muscles are unknown. Using in situ hybridization histochemistry, we examined spatiotemporal expression patterns of gp130, IL-6R, LIFR, and CNTFR mRNAs in regenerating muscles after muscle contusion. At the early stages of regeneration (from 3 hr to Day 2 post contusion), significant signals for gp130 and LIFR mRNAs were detected in myonuclei and/or nuclei of muscle precursor cells (mpcs) and in mononuclear cells located in extracellular spaces between myofibers after muscle contusion, but IL-6R mRNA was expressed only in mononuclear cells. At Day 7 post contusion, signals for gp130, LIFR, and IL-6R mRNAs were not detected in newly formed myotubes, whereas the CNTFR mRNA level was upregulated in myotubes. These findings suggest that the upregulation of receptor subunits in distinct cell populations plays an important role in the effective regeneration of both myofibers and motor neurons.

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Section: Discussionmentioning

confidence: 99%

Gene Expression of Receptors for IL-6, LIF, and CNTF in Regenerating Skeletal Muscles

Kami

Morikawa²,

Sekimoto³

et al. 2000

J Histochem Cytochem.

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“…What is its role within the muscle is to be clarified further. Finally, LIF is a pleiotropic cytokine that has been suggested to have positive effects on myogenesis (38) by increasing survival of myoblasts (39).…”

Section: The Myokinesmentioning

confidence: 99%

Skeletal muscle: an endocrine organ

Pratesi

Tarantini²,

Bari³

2013

CCMBM

123

113

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SummaryTropism and efficiency of skeletal muscle depend on the complex balance between anabolic and catabolic factors. This balance gradually deteriorates with aging, leading to an age-related decline in muscle quantity and quality, called sarcopenia: this condition plays a central role in physical and functional impairment in late life. The knowledge of the mechanisms that induce sarcopenia and the ability to prevent or counteract them, therefore, can greatly contribute to the prevention of disability and probably also mortality in the elderly. It is well known that skeletal muscle is the target of numerous hormones, but only in recent years studies have shown a role of skeletal muscle as a secretory organ of cytokines and other peptides, denominated myokines (IL6, IL8, IL15, Brain-derived neurotrophic factor, and leukaemia inhibitory factor), which have autocrine, paracrine, or endocrine actions and are deeply involved in inflammatory processes. Physical inactivity promotes an unbalance between these substances towards a pro-inflammatory status, thus favoring the vicious circle of sarcopenia, accumulation of fat -especially visceral -and development of cardiovascular diseases, type 2 diabetes mellitus, cancer, dementia and depression, according to what has been called "the diseasome of physical inactivity".

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“…Recently, IL-6 was also found to be required for the overload-induced muscle hypertrophy [72]. In addition, LIF is known to promote myoblast proliferation and plays an essential role in the injury-induced muscle regeneration [73][74][75][76][77]. Among members of the IL-6 family, OSM is most closely related to LIF.…”

Section: Multiple Members Of the Il-6 Family Regulate Myoblast Differmentioning

confidence: 99%

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

Xiao

Wang

et al. 2010

Cell Res

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Oncostatin M (OSM) is a cytokine of the interleukin-6 family and plays important roles during inflammation. However, its roles in myoblast differentiation and muscle regeneration remain unexplored. We show here that OSM potently inhibited myoblast differentiation mainly by activating the JAK1/STAT1/STAT3 pathway. OSM downregulated myocyte enhancer-binding factor 2A (MEF2A), upregulated the expression of Id1 and Id2, and inhibited the transcriptional activity of MyoD and MEF2. In addition, OSM also enhanced the expression of STAT3 and OSM receptor, which constituted a positive feedback loop to further amplify OSM-induced signaling. Moreover, we found that STAT1 physically associated with MEF2 and repressed its transcriptional activity, which could account for the OSM-mediated repression of MEF2. Although undetectable in normal muscles in vivo, OSM was rapidly induced on muscle injury and then promptly downregulated just before the majority of myoblasts differentiate. Prolonged expression of OSM in muscles compromised the regeneration process without affecting myoblast proliferation, suggesting that OSM functions to prevent proliferating myoblasts from premature differentiation during the early phase of muscle regeneration.

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Effects of leukaemia inhibitory factor and other cytokines on murine and human myoblast proliferation

Cited by 113 publications

References 8 publications

Gene Expression of Receptors for IL-6, LIF, and CNTF in Regenerating Skeletal Muscles

Gene Expression of Receptors for IL-6, LIF, and CNTF in Regenerating Skeletal Muscles

Skeletal muscle: an endocrine organ

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

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