Tumor necrosis factor induces skeletal muscle protein breakdown in rats

Goodman, M. N.

doi:10.1152/ajpendo.1991.260.5.e727

Cited by 159 publications

(148 citation statements)

References 9 publications

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“…Skeletal muscle fibers have been shown to produce TNFα in a fiber type specific manner in both humans (Plomgaard et al, 2005) and rats (Phillips and Leeuwenburgh, 2005). TNFα is associated with accelerated skeletal muscle protein loss both in vitro (Li and Reid, 2000) and in vivo (Flores et al, 1989;Goodman, 1991). In the present study, we found that the absence of IL-10 was associated with a significantly greater plasma TNFα response, but that this did not extend to an increase in skeletal muscle content of TNFα.…”

Section: Discussionsupporting

confidence: 39%

Exaggerated expression of skeletal muscle-derived interleukin-6, but not TNFα, in mice lacking interleukin-10

Huey

McCusker

Kelley

2008

Journal of Neuroimmunology

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IL-10 reduces cytokine expression in non-muscle tissues, but its effect on skeletal muscle remains undefined. Therefore, we tested the hypothesis that endogenous IL-10 acts to reduce cytokines in the gastrocnemius muscle by comparing IL-6 and TNFα expression in wild-type (IL-10 +/+ ) and IL-10 deficient (IL-10 −/− ) mice following an inflammatory insult induced by peripheral LPS. IL-6 mRNA expression increased following LPS for both IL-10 +/+ and IL-10 −/− mice; the response was greater and prolonged in IL-10 −/− mice. Muscle TNFα mRNA also increased, but without differences between genotypes. IL-6 protein concentrations were elevated by LPS with a greater and prolonged response for IL-10 −/− mice, but TNFα did not change. These results provide the first in vivo evidence that endogenous IL-10 attenuates IL-6 expression by skeletal muscle in response to LPS.

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Section: Discussionsupporting

confidence: 39%

Exaggerated expression of skeletal muscle-derived interleukin-6, but not TNFα, in mice lacking interleukin-10

Huey

McCusker

Kelley

2008

Journal of Neuroimmunology

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“…tumour necrosis factor-a (TNF-a)) have also been implicated in the skeletal muscle atrophy of several physiological/ pathological states. 37,38 In animals treated with exogenous TNF-a 38,39 or expressing a transgene, 40 losses in muscle mass are observed. Moreover, Buck and Chojkier 39 reported structural irregularities consisting of smaller fibres in skeletal muscles from mice receiving exogenous TNF-a.…”

Section: Iiamentioning

confidence: 99%

Morphological and biochemical alterations of skeletal muscles from the genetically obese (ob/ob) mouse

et al. 2009

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Background: Knowledge of the morphological and biochemical alterations occurring in skeletal muscles of obese animals is relatively limited, particularly with respect to non-limb muscles and relationship to fibre type. Objective: Sternomastoid (SM; fast-twitch), extensor digitorum longus (EDL; fast-twitch), and soleus (SOL; mixed) muscles of ob/ob mouse (18-22 weeks) were examined with respect to size (mass, muscle mass-to-body mass ratio, cross-sectional area (CSA)), fibre CSA, protein content, myosin heavy chain (MHC) content, MHC isoform (MHC i ) composition, MHC i -based fibre type composition, and lactate dehydrogenase isoenzyme (LDH iso ) composition. Results: Compared with (control) muscles from lean mice, all the three muscles from ob/ob mice were smaller in size (by 13-30%), with SM and EDL being the most affected. The CSA of IIB and IIB þ IID fibres (the predominant fibre types in SM and EDL muscles) was markedly smaller (by B30%) in ob/ob mice, consistent with differences in muscle size. Total protein content (normalised to muscle mass) was significantly lower in EDL (À9.7%) and SOL (À14.1%) muscles of ob/ob mice, but there were no differences between SM, EDL, and SOL muscles from the two animal groups with respect to MHC content (also normalised to muscle mass). Electrophoretic analyses of MHC i composition in whole muscle homogenates and single muscle fibres showed a shift towards slower MHC i content, slower MHC i containing fibres, and a greater proportion of hybrid fibres in all the three muscles of ob/ob mice, with a shift towards a more aerobic-oxidative phenotype also observed with respect to LDH iso composition. Conclusion: This study showed that SM, EDL, and SOL muscles of ob/ob mice display size reductions to an extent that seems to be largely related to fibre type composition, and a shift in fibre type composition that may result from a process of structural remodelling, as suggested by the increased proportion of hybrid fibres in muscles of ob/ob mice.

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“…Muscle structure and cell surface and extracellular cytoskeleton up-regulated genes found in both JDM and DMD, including embryonic myosin heavy chain (52.5-fold), myosin-binding protein H (71.3-fold), skeletal muscle perinatal myosin heavy chain MYH8 (13.9-fold), nicotinic acetylcholine receptor ␣ subunit (12.2-fold), thrombospondin-4 (8.2-fold), prepro-␣2 (I) collagen (7.4-fold), and chondroitin sulfate proteoglycan versican (ϳ5-fold). TNF-␣ release is a feature of necrotic muscle, and TNF-␣ itself damages skeletal muscle (43).…”

Section: Degeneration/regeneration Cascades Expressed By Necrotic Myomentioning

confidence: 99%

Gene Expression Profiling in DQA1*0501+ Children with Untreated Dermatomyositis: A Novel Model of Pathogenesis

Težak

Hoffman

Lutz³

et al. 2002

The Journal of Immunology

222

143

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Juvenile dermatomyositis (JDM), the most common pediatric inflammatory myopathy, is a systemic vasculopathy affecting young children. Epidemiology studies documenting an antecedent illness in the 3 mo before the first definite symptom (rash and/or weakness) of JDM are supported by immunologic data that suggest that the disease pathophysiology is Ag driven. The purpose of this study was to compare the gene expression profiles in muscle biopsies of four untreated DQA1*0501+ JDM children with profiles from children with a known necrotizing myopathy (Duchenne muscular dystrophy), as well as an in vitro antiviral model (NF90), and healthy pediatric controls. Nearly half (47%) of the dysregulated genes in JDM were associated with the immune response. In particular, increased expression of IFN-αβ-inducible genes 6-16, myxovirus resistance protein p78, latent cytosolic transcription factor, LMP2, and TAP1 was observed. This profile is consistent with an IFN-αβ transcription cascade seen in the in vitro viral resistance model. The IFN-αβ-inducible profile was superimposed on transcription profiles reflective of myofiber necrosis and regeneration shared with Duchenne muscular dystrophy. Expressed genes were confirmed by quantitative real-time PCR (6-16), immunofluorescence (thrombospondin 4), and immunolocalization (IFN-γ, p21). We hypothesize that these data support a model of Ag (?viral) induction of an apparent autoimmune disease based on dynamic interaction between the muscle, vascular, and immune systems in the genetically susceptible (DQA1*0501+) child.

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Tumor necrosis factor induces skeletal muscle protein breakdown in rats

Cited by 159 publications

References 9 publications

Exaggerated expression of skeletal muscle-derived interleukin-6, but not TNFα, in mice lacking interleukin-10

Exaggerated expression of skeletal muscle-derived interleukin-6, but not TNFα, in mice lacking interleukin-10

Morphological and biochemical alterations of skeletal muscles from the genetically obese (ob/ob) mouse

Gene Expression Profiling in DQA1*0501+ Children with Untreated Dermatomyositis: A Novel Model of Pathogenesis

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