Leukemia inhibitory factor (LIF) infusion stimulates skeletal muscle regeneration after injury: Injured muscle expresses lif mRNA

Barnard, W.; Bower, J.; Brown, Melissa A.; Murphy, Mark; Austin, L.

doi:10.1016/0022-510x(94)90211-9

Cited by 123 publications

(95 citation statements)

References 12 publications

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“…LIF is expressed following muscle injury and is necessary for muscle regeneration (40,41). LIF was shown to promote proliferation and inhibit differentiation of C2C12 and primary myoblasts (42,43).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Myoblast Differentiation by Tumor Necrosis Factor α Is Mediated by c-Jun N-terminal Kinase 1 and Leukemia Inhibitory Factor

Alter

Rozentzweig

Bengal

2008

Journal of Biological Chemistry

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The proinflammatory cytokine, TNF␣ plays a major role in muscle wasting occurring in chronic diseases and muscular dystrophies. Among its other functions, TNF␣ perturbs muscle regeneration by preventing satellite cell differentiation. In the present study, the role of c-Jun N-terminal kinase (JNK), a mediator of TNF␣, was investigated in differentiating myoblast cell lines. Addition of TNF␣ to C2 myoblasts induced immediate and delayed phases of JNK activity. The delayed phase is associated with myoblast proliferation. Inhibition of JNK activity prevented proliferation and restored differentiation to TNF␣-treated myoblasts. Studies with cell lines expressing MyoD:ER chimera and lacking JNK1 or JNK2 genes indicate that JNK1 activity mediates the effects of TNF␣ on myoblast proliferation and differentiation. TNF␣ does not induce proliferation or inhibit differentiation of JNK1-null myoblasts. However, differentiation of JNK1-null myoblasts is inhibited when they are grown in conditioned medium derived from cell lines affected by TNF␣. We investigated the induced synthesis of several candidate growth factors and cytokines following treatment with TNF␣. Expression of IL-6 and leukemia inhibitory factor (LIF) was induced by TNF␣ in wildtype and JNK2-null myoblasts. However, LIF expression was not induced by TNF␣ in JNK1-null myoblasts. Addition of LIF to the growth medium of JNK1-null myoblasts prevented their differentiation. Moreover, LIF-neutralizing antibodies added to the medium of C2 myoblasts prevented inhibition of differentiation mediated by TNF␣. Hence, TNF␣ promotes myoblast proliferation through JNK1 and prevents myoblast differentiation through JNK1-mediated secretion of LIF.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Myoblast Differentiation by Tumor Necrosis Factor α Is Mediated by c-Jun N-terminal Kinase 1 and Leukemia Inhibitory Factor

Alter

Rozentzweig

Bengal

2008

Journal of Biological Chemistry

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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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“…Delivery of exogenous LIF to acutely injured muscle increased muscle regeneration (135), and mice that were null mutants for LIF showed slower muscle repair following injury than wild-type mice (136). In addition, exogenous LIF prevented muscle atrophy that occurred after muscle denervation (137).…”

Section: Delivery Of Mitogens To Musclementioning

confidence: 99%

Evolving Therapeutic Strategies for Duchenne Muscular Dystrophy: Targeting Downstream Events

Tidball¹,

Wehling‐Henricks

2004

Pediatr Res

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Leukemia inhibitory factor (LIF) infusion stimulates skeletal muscle regeneration after injury: Injured muscle expresses lif mRNA

Cited by 123 publications

References 12 publications

Inhibition of Myoblast Differentiation by Tumor Necrosis Factor α Is Mediated by c-Jun N-terminal Kinase 1 and Leukemia Inhibitory Factor

Inhibition of Myoblast Differentiation by Tumor Necrosis Factor α Is Mediated by c-Jun N-terminal Kinase 1 and Leukemia Inhibitory Factor

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

Evolving Therapeutic Strategies for Duchenne Muscular Dystrophy: Targeting Downstream Events

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