Stimulation of myoblast proliferation in culture by leukaemia inhibitory factor and other cytokines

Austin, L.; Burgess, Antony W.

doi:10.1016/0022-510x(91)90045-9

Cited by 142 publications

(78 citation statements)

References 13 publications

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“…LIF was shown to promote proliferation and inhibit differentiation of C2C12 and primary myoblasts (42,43). Signaling molecules like Stat3 (44) and ERK MAPK (45) Understanding the inhibitory effect of LIF on myoblast differentiation may extend beyond this particular process and lead to the understanding of how LIF can preserve multipotentiality of embryonic as well as adult stem cells.…”

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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“…IL-6 also stimulates myoblast proliferation (Austin and Burgess 1991) and is a candidate for upregulation in the absence of TNF-␣. Another cytokine that may be of importance in muscle regeneration in the absence of TNF-␣ is transforming growth factor-beta (TGF-␤) (Derynck and Choy 1998).…”

Section: Cytokine Interactionsmentioning

confidence: 99%

The Role of Tumor Necrosis Factor-alpha (TNF-α) in Skeletal Muscle Regeneration

Collins

Grounds²

2001

J Histochem Cytochem.

147

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The role of tumor necrosis factor-alpha (TNF-α), an important mediator of the inflammatory response after injury, was investigated in regenerating skeletal muscle. The pattern of expression of TNF-α during muscle regeneration was examined by immunohistochemistry in tissue sections of crush-injured or transplanted muscle autografts and in primary cultures of adult skeletal muscle. TNF-α was highly expressed in injured myofibers, inflammatory cells, endothelial cells, fibroblasts, and mast cells. Myoblasts and myotubes also expressed TNF-α in primary muscle cultures and tissue sections. The essential role of TNF-α and its homologue lymphotoxin-alpha (LT-α) during muscle regeneration was assessed by basic histology in TNF-α(–) and TNF-α(-/-)/LT-α(-/-) mice. No difference was apparent in the onset or pattern of muscle regeneration (i.e., inflammatory response, activation and fusion of myoblasts) between the two strains of null mice or between nulls and normal control mice. However, both strains of null mice appeared more prone to bystander damage of host muscle and regeneration distant from the site of injury/transplantation. Although expression of TNF-α may play an important role in muscle regeneration, the studies in the null mice show that redundancy within the cytokine system (or some other response) can effectively compensate for the absence of TNF-α in vivo. (J Histochem Cytochem 49:989–1001, 2001)

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“…The cytokines IL-6, leukemia inhibitory factor (LIF), and TGF␣ can stimulate muscle progenitor proliferation and inhibit their differentiation in culture (Austin and Burgess 1991;Austin et al 1992;Jo et al 2005), but IL-6 KO mice have no muscle regeneration defect (Warren et al 2002), making it unclear at present whether these cytokines play a role in vivo. TNF receptor double-knockout mice and mice treated with neutralizing anti-TNF␣ antibody show defects in expression of muscle differentiation markers and in formation of new muscle fibers (Warren et al 2002;Chen et al 2005), indicating that TNF␣ signaling has a positive role in muscle regeneration.…”

Section: Cytokine Signalingmentioning

confidence: 99%

Advances in signaling in vertebrate regeneration as a prelude to regenerative medicine

Stoick-Cooper¹,

Moon²,

Weidinger³

2007

Genes Dev.

276

278

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While all animals have evolved strategies to respond to injury and disease, their ability to functionally recover from loss of or damage to organs or appendages varies widely damage to skeletal muscle, but, unlike amphibians and fish, they fail to regenerate heart, lens, retina, or appendages. The relatively young field of regenerative medicine strives to develop therapies aimed at improving regenerative processes in humans and is predicated on >40 years of success with bone marrow transplants. Further progress will be accelerated by implementing knowledge about the molecular mechanisms that regulate regenerative processes in model organisms that naturally possess the ability to regenerate organs and/or appendages. In this review we summarize the current knowledge about the signaling pathways that regulate regeneration of amphibian and fish appendages, fish heart, and mammalian liver and skeletal muscle. While the cellular mechanisms and the cell types involved in regeneration of these systems vary widely, it is evident that shared signals are involved in tissue regeneration. Signals provided by the immune system appear to act as triggers of many regenerative processes. Subsequently, pathways that are best known for their importance in regulating embryonic development, in particular fibroblast growth factor (FGF) and Wnt/␤-catenin signaling (as well as others), are required for progenitor cell formation or activation and for cell proliferation and specification leading to tissue regrowth. Experimental activation of these pathways or interference with signals that inhibit regenerative processes can augment or even trigger regeneration in certain contexts.

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Stimulation of myoblast proliferation in culture by leukaemia inhibitory factor and other cytokines

Cited by 142 publications

References 13 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

The Role of Tumor Necrosis Factor-alpha (TNF-α) in Skeletal Muscle Regeneration

Advances in signaling in vertebrate regeneration as a prelude to regenerative medicine

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