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

Alter, Joel; Rozentzweig, Dafna; Bengal, Eyal

doi:10.1074/jbc.m801379200

Cited by 70 publications

(61 citation statements)

References 47 publications

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“…1C and previously published results , suggesting that the factors or cytokines secreted by inflammatory cells such as neutrophils and macrophages may regulate miR-128a expression. TNF-a is a major pro-inflammatory cytokine that plays an important role in muscle regeneration by promoting myoblast proliferation and differentiation (Alter et al, 2008;Chen et al, 2007;Li, 2003;Li and Schwartz, 2001;Warren et al, 2002). TNF-a expression is upregulated immediately following CTX injection in mouse muscles (Chen et al, 2007).…”

Section: Inhibition Of Mir-128 By Minicircle Vectors Induced Muscle Hmentioning

confidence: 99%

“…TNF-a expression is upregulated immediately following CTX injection in mouse muscles (Chen et al, 2007). Furthermore, TNF-a is also known to regulate miR-128a by targeting the adenosine 2B receptor (A2BAR) in epithelial cells (Kolachala et al, 2010), which in turn regulates insulin signaling and myoblast proliferation (Alter et al, 2008;Li, 2003;Yamasaki et al, 1996). We first examined the effects of TNF-a on miR-128a expression in myoblasts.…”

Section: Inhibition Of Mir-128 By Minicircle Vectors Induced Muscle Hmentioning

confidence: 99%

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Regulation of IRS1/Akt insulin signaling by microRNA-128a during myogenesis

Matsuki

Alexander

Shimizu‐Motohashi

et al. 2013

Journal of Cell Science

114

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SummarySkeletal muscle possesses a strong ability to regenerate following injury, a fact that has been largely attributed to satellite cells. Satellite cells are skeletal muscle stem cells located beneath the basal lamina of the myofiber, and are the principal cellular source of growth and regeneration in skeletal muscle. MicroRNAs (miRNAs) play key roles in modulating several cellular processes by targeting multiple mRNAs that comprise a single or multiple signaling pathway. Several miRNAs have been shown to regulate satellite cell activity, such as miRNA-489, which functions to maintain satellite cells in a quiescent state. Although muscle-specific miRNAs have been identified, many of the molecular mechanisms that regulate myogenesis that are regulated by miRNAs still remain unknown. In this study, we have shown that miR-128a is highly expressed in brain and skeletal muscle, and increases during myoblast differentiation. MiR-128a was found to regulate the target genes involved in insulin signaling, which include Insr (insulin receptor), Irs1 (insulin receptor substrate 1) and Pik3r1 (phosphatidylinositol 3-kinases regulatory 1) at both the mRNA and protein level. Overexpression of miR-128a in myoblasts inhibited cell proliferation by targeting IRS1. By contrast, inhibition of miR-128a induced myotube maturation and myofiber hypertrophy in vitro and in vivo. Moreover, our results demonstrate that miR-128a expression levels are negatively controlled by tumor necrosis factor a (TNF-a). TNF-a promoted myoblast proliferation and myotube hypertrophy by facilitating IRS1/Akt signaling via a direct decrease of miR-128a expression in both myoblasts and myotubes. In summary, we demonstrate that miR-128a regulates myoblast proliferation and myotube hypertrophy, and provides a novel mechanism through which IRS1-dependent insulin signaling is regulated in skeletal muscle.

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Section: Inhibition Of Mir-128 By Minicircle Vectors Induced Muscle Hmentioning

confidence: 99%

Section: Inhibition Of Mir-128 By Minicircle Vectors Induced Muscle Hmentioning

confidence: 99%

Regulation of IRS1/Akt insulin signaling by microRNA-128a during myogenesis

Matsuki

Alexander

Shimizu‐Motohashi

et al. 2013

Journal of Cell Science

114

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“…For example, treating myoblasts with IL-10 prevented the induction of JNK phosphorylation by TNFα-activated pathways (Strle et al, 2007). Because TNFα can promote satellite cell proliferation and inhibit differentiation through a JNK-mediated pathway in addition to the NFκB and p38 MAPK pathways (Alter et al, 2008), IL-10 may contribute to the transition from the proliferative stage of myogenesis to early differentiation by inhibiting TNFα induction of JNK in myogenic cells. In vivo observations show that stages of inflammation and stages of muscle regeneration can be synchronized by IL-10 that is likely to be derived from macrophages.…”

Section: Role Of Il-10-mediated Signalingmentioning

confidence: 99%

Shared signaling systems in myeloid cell-mediated muscle regeneration

2014

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Much of the focus in muscle regeneration has been placed on the identification and delivery of stem cells to promote regenerative capacity. As those efforts have advanced, we have learned that complex features of the microenvironment in which regeneration occurs can determine success or failure. The immune system is an important contributor to that complexity and can determine the extent to which muscle regeneration succeeds. Immune cells of the myeloid lineage play major regulatory roles in tissue regeneration through two general, inductive mechanisms: instructive mechanisms that act directly on muscle cells; and permissive mechanisms that act indirectly to influence regeneration by modulating angiogenesis and fibrosis. In this article, recent discoveries that identify inductive actions of specific populations of myeloid cells on muscle regeneration are presented, with an emphasis on how processes in muscle and myeloid cells are co-regulated. KEY WORDS: Muscle regeneration, Macrophage phenotype, Signaling systems IntroductionAcute trauma, chronic disease or disruption of vascularization cause rapid death of skeletal muscle. Functional recovery of the damaged tissue is determined by interacting cellular responses, including stem cell activation, proliferation and differentiation, vascular repair, and tissue fibrosis during healing. Experimental approaches to improve muscle regeneration have focused on identifying stem cell populations that promote regeneration and refining their delivery, while using genetic or pharmacological manipulations to influence angiogenesis and fibrosis. However, those approaches are sensitive to the presence of myeloid cells in the injured muscle, suggesting that manipulations of myeloid cells can provide novel strategies to potentiate muscle regeneration. As knowledge of myeloid cell involvement in muscle regeneration has grown, we have come to appreciate that multiple subpopulations interact in complex and delicately balanced ways to influence regeneration. Perturbations in myeloid cell number, phenotype or the stage of regeneration at which they are present can yield vastly different outcomes in the regenerative process. As these complexities become better understood, there is hope that knowledge can be exploited to improve muscle regeneration therapy.In this Review, inductive processes through which myeloid cells influence muscle regeneration are presented, including instructive processes that directly influence developmental gene expression in muscle and permissive processes that modify the environment in which regeneration occurs. Here, muscle 'regeneration' refers to processes in damaged muscle tissue that lead to the restoration of normal structure and homeostasis, especially those events that influence the differentiation and growth of muscle cells that replace damaged tissue (Box 1). In addition, we emphasize discoveries that have contributed to understanding the mechanisms that coordinate phenotypic switches in myeloid cell populations with progressive stages of musc...

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“…This effect was counteracted by the overexpression of necdin in C2C12 and MlcNec myoblasts and enhanced by necdin ablation (Ndn -/-myoblasts). TNFα significantly contributes to cachexia (Zhou et al, 2003;Coletti et al, 2005); in addition, low concentrations of TNFα inhibit myogenic differentiation without causing apoptosis, which ensues at high concentrations of the cytokine (Alter et al, 2008;Coletti et al, 2002;Moresi et al, 2008). Oxidative stress (reactive oxygen species, ROS) accompanies and sustains the action of TNFα (Barreiro et al, 2005;Li et al, 2003).…”

Section: Necdin Is a Physiological Inhibitor Of Colon-carcinoma-inducmentioning

confidence: 99%

Necdin is expressed in cachectic skeletal muscle to protect fibers from tumor-induced wasting

Sciorati¹,

Touvier²,

Buono³

et al. 2009

Journal of Cell Science

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Skeletal muscles of subjects with advanced cancer undergo progressive wasting, referred to as cachexia. Cachexia is an important area for medical research because strategies proposed until now have yielded little benefit. We have recently identified necdin as a key player in fetal and postnatal physiological myogenesis and in muscle regeneration. Here we show that necdin is selectively expressed in muscles of cachetic mice and prove that its expression is causally linked to a protective response of the tissue against tumor-induced wasting, inhibition of myogenic differentiation and fiber regeneration. Necdin carries out this role mainly via interference with TNFα signaling at various levels, including regulation of expression of TNFR1 and p53, and regulation of the activity of caspase 3 and caspase 9. These data suggest that inhibition of muscle wasting using necdin is a feasible approach to treat cachexia in neoplastic patients.

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

Cited by 70 publications

References 47 publications

Regulation of IRS1/Akt insulin signaling by microRNA-128a during myogenesis

Regulation of IRS1/Akt insulin signaling by microRNA-128a during myogenesis

Shared signaling systems in myeloid cell-mediated muscle regeneration

Necdin is expressed in cachectic skeletal muscle to protect fibers from tumor-induced wasting

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