NF-κB-Mediated MyoD Decay during Muscle Wasting Requires Nitric Oxide Synthase mRNA Stabilization, HuR Protein, and Nitric Oxide Release

Marco, Sergio Di; Mazrouï, Rachid; Dallaire, Patrice; Chittur, Sridar V.; Tenenbaum, Scott A.; Radzioch, Danuta; Marette, André; Gallouzi, Imed Eddine

doi:10.1128/mcb.25.15.6533-6545.2005

Cited by 142 publications

(180 citation statements)

References 63 publications

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“…TNF‐α promotes myoblast proliferation at early stages of myogenesis while repressing myoblast differentiation (Chen et al, 2007; Guttridge et al, 2000; Langen et al, 2001; Li, 2003). Administration of TNF‐α to primary myoblast cultures increased number of primary myoblasts incorporating BrdU (Li, 2003) and increased myoblast proliferation in C2C12 cultures (Alvarez et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…In response to injury, satellite cells exit their quiescent state and then proliferate, differentiate, and fuse with existing myofibers to provide new myonuclei and replace or repair injured cells (Relaix & Zammit, 2012). These regenerative functions of satellite cells can be affected by TNF‐α which reduces myogenic differentiation through transcriptional activation of NF‐κB and decreases protein stability of MyoD, a transcription factor that plays a key role in regulating myoblast transition from proliferation to differentiation (Guttridge, Mayo, Madrid, Wang, & Baldwin, 2000; Langen et al, 2004). In addition, in vitro observations show that TNF‐α has bimodal effects on myogenesis, promoting myoblast proliferation at early stages of myogenesis while repressing myoblast differentiation (Chen, Jin, & Li, 2007; Langen, Schols, Kelders, Wouters, & Janssen‐Heininger, 2001; Palacios et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Myeloid cell‐derived tumor necrosis factor‐alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

et al. 2018

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Sarcopenia is age‐related muscle wasting that lacks effective therapeutic interventions. We found that systemic ablation of tumor necrosis factor‐α (TNF‐α) prevented sarcopenia and prevented age‐related change in muscle fiber phenotype. Furthermore, TNF‐α ablation reduced the number of satellite cells in aging muscle and promoted muscle cell fusion in vivo and in vitro. Because CD68+ macrophages are important sources of TNF‐α and the number of CD68+ macrophages increases in aging muscle, we tested whether macrophage‐derived TNF‐α affects myogenesis. Media conditioned by TNF‐α‐null macrophages increased muscle cell fusion in vitro, compared to media conditioned by wild‐type macrophages. In addition, transplantation of bone marrow cells from wild‐type mice into TNF‐α‐null recipients increased satellite cell numbers and reduced numbers of centrally nucleated myofibers, indicating that myeloid cell‐secreted TNF‐α reduces muscle cell fusion. Transplanting bone marrow cells from wild‐type mice into TNF‐α‐null recipients also increased sarcopenia, although transplantation did not restore the age‐related change in muscle fiber phenotype. Collectively, we show that myeloid cell‐derived TNF‐α contributes to muscle aging by affecting sarcopenia and muscle cell fusion with aging muscle fibers. Our findings also show that TNF‐α that is intrinsic to muscle and TNF‐α secreted by immune cells work together to influence muscle aging.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Myeloid cell‐derived tumor necrosis factor‐alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

et al. 2018

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“…Our results support a model whereby macrophages recruited to muscle injury are M2 polarized by the regenerating environment to stimulate fiber growth; thus a mutation that specifically impairs M2-specific macrophage gene expression interferes with the later stages of muscle regeneration and fiber replacement, whereas the initial removal of necrotic tissue is maintained. Specifically, the reduction of Arg-1 expression in ␤⌬Cre macrophages is likely to result in the re-routing of arginine metabolism away from arginasemediated polyamine synthesis (which promotes tissue regeneration) toward iNOS-mediated NO production (which promotes degradation of transcripts encoding the myocyte differentiation factor MyoD) (26). An essential CREB-dependent pathway for inducing Arg-1 and polyamine synthesis during axonal regeneration has previously been described (27).…”

Section: Discussionmentioning

confidence: 99%

A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair

Ruffell

Mourkioti²,

Gambardella³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

549

439

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Macrophages play an essential role in the resolution of tissue damage through removal of necrotic cells, thus paving the way for tissue regeneration. Macrophages also directly support the formation of new tissue to replace the injury, through their acquisition of an anti-inflammatory, or M2, phenotype, characterized by a gene expression program that includes IL-10, the IL-13 receptor, and arginase 1. We report that deletion of two CREB-binding sites from the Cebpb promoter abrogates Cebpb induction upon macrophage activation. This blocks the downstream induction of M2-specific Msr1, Il10, II13ra, and Arg-1 genes, whereas the inflammatory (M1) genes Il1, Il6, Tnfa, and Il12 are not affected. Mice carrying the mutated Cebpb promoter (␤⌬Cre) remove necrotic tissue from injured muscle, but exhibit severe defects in muscle fiber regeneration. Conditional deletion of the Cebpb gene in muscle cells does not affect regeneration, showing that the C/EBP␤ cascade leading to muscle repair is muscle-extrinsic. While ␤⌬Cre macrophages efficiently infiltrate injured muscle they fail to upregulate Cebpb, leading to decreased Arg-1 expression. CREB-mediated induction of Cebpb expression is therefore required in infiltrating macrophages for upregulation of M2-specific genes and muscle regeneration, providing a direct genetic link between these two processes.macrophage polarization ͉ muscle regeneration ͉ transcription

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“…Our preliminary data suggest that AMPK is implicated in the regulation of AM mRNA expression by glucose concentration (data not shown), in accordance with previous reports, 10,11 and that stability of AM mRNA may not be involved in this regulation, in contrast to a previous report. 12 Tumor cells were implanted s.c. in the back of SCID mice and grown to B5 mm in diameter. On day 9, 500 mg naked DNA encoding AMA was injected into the tumor tissues.…”

Section: Resultsmentioning

confidence: 99%

Suppression of tumor growth by intra-muscular transfer of naked DNA encoding adrenomedullin antagonist

et al. 2006

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We have recently reported that the intra-tumoral injection of adrenomedullin (AM) antagonist (AMA; AM (22-52)) peptides significantly reduced the in vivo growth of a pancreatic cancer cell line in severely combined immunodeficient (SCID) mice. In the present study, we examined the effects of intra-tumoral and intra-muscular transfers of naked DNA encoding AMA on the in vivo growth of cancer cell lines. We demonstrate that these treatments induce the regression of a pancreatic cancer cell line and a breast cancer cell line inoculated in SCID mice. Furthermore, CD31-positive cells disappear completely from tumor tissues, following treatment, indicating that neo-vascularization is entirely inhibited. These results suggest that the intra-tumoral or intra-muscular transfer of naked DNA encoding AMA might be a promising alternative modality for treating human cancers.

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NF-κB-Mediated MyoD Decay during Muscle Wasting Requires Nitric Oxide Synthase mRNA Stabilization, HuR Protein, and Nitric Oxide Release

Cited by 142 publications

References 63 publications

Myeloid cell‐derived tumor necrosis factor‐alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

Myeloid cell‐derived tumor necrosis factor‐alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair

Suppression of tumor growth by intra-muscular transfer of naked DNA encoding adrenomedullin antagonist

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