Novel activity of an anti-inflammatory cytokine: IL-10 prevents TNFα-induced resistance to IGF-I in myoblasts

Strle, Klemen; McCusker, Robert H.; Tran, Lynn; King, A C; Johnson, Rodney W.; Freund, Gregory G.; Dantzer, Robert; Kelley, Keith W.

doi:10.1016/j.jneuroim.2007.05.003

Cited by 35 publications

(24 citation statements)

References 36 publications

(56 reference statements)

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“…The relatively higher amounts of IL-10 in CM-LPS compared with CM-P might counteract the relatively lower amounts of TNF␣ and IL-6 and other proinflammatory cytokines present in CM-LPS compared with CM-P. Future studies should define their combined contribution and whether phospho-JNK is responsible for the insulin resistance elicited by CM-P. Regarding the latter, exposure of C 2 C 12 muscle cells to IL-10 diminished the stimulation of JNK phosphorylation by TNF␣ or IL-1␤ (40,41).…”

Section: Discussionmentioning

confidence: 99%

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Samokhvalov¹,

Bilan²,

Schertzer³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Section: Discussionmentioning

confidence: 99%

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Samokhvalov¹,

Bilan²,

Schertzer³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…GH and IL6 receptors belong to the class I cytokine receptors, which show structural similarities and share intracellular regulatory pathways, thereby implying the possibility of various intracellular interactions between IL6, GH, and their receptors (45,46). For IGF1, similar intracellular cross talks have been suggested primarily linking IGF1 and TNFa activity (4,8,42).…”

Section: Discussionmentioning

confidence: 99%

“…The vast majority of clinical and experimental studies have focused on stages with increased inflammation where it seems that chronic inflammation suppresses the GH/IGF1 axis (2,5,6,7,8,9). In addition, more recent observations have demonstrated that the relationship may be bidirectional, with GH/IGF1 activity influencing inflammatory processes (3,10,11).…”

Section: Introductionmentioning

confidence: 99%

GH activity and markers of inflammation: a crossover study in healthy volunteers treated with GH and a GH receptor antagonist

Andreassen

Frystyk

Faber

et al. 2012

European Journal of Endocrinology

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Introduction: The GH/IGF1 axis may modulate inflammatory processes. However, the relationship seems complicated as both pro-and anti-inflammatory effects have been demonstrated. Methods/design: Twelve healthy volunteers (mean age 36, range 27-49 years) were treated in random order with increasing doses of GH for 3 weeks (first week 0.01 mg/kg per day, second week 0.02 mg/kg per day, and third week 0.03 mg/kg per day) or a GH receptor antagonist (pegvisomant; first week 10 mg/day and last two weeks 15 mg/day), separated by 8 weeks of washout. Circulating levels of the pro-inflammatory cytokines tumor necrosis factor a (TNFa (TNFA)), interleukin 6 (IL6), and IL1b (IL1B) and the acute phase proteins (APPs) C-reactive protein (CRP), haptoglobin, orosomucoid, YKL40 (CHI3L1), and fibrinogen were measured. Conclusions: GH/IGF1 action appears to modulate the initial stage of the inflammatory response as well as downstream processes elucidated by levels of APPs. The data suggest a complicated relationship not allowing any simple conclusions as to whether GH/IGF1 actions have mainly pro-or antiinflammatory effects in vivo.

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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.…”

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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Novel activity of an anti-inflammatory cytokine: IL-10 prevents TNFα-induced resistance to IGF-I in myoblasts

Cited by 35 publications

References 36 publications

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells

GH activity and markers of inflammation: a crossover study in healthy volunteers treated with GH and a GH receptor antagonist

Shared signaling systems in myeloid cell-mediated muscle regeneration

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