Expression of tumor necrosis factor-α in regenerating muscle fibers in inflammatory and non-inflammatory myopathies

Kuru, Satoshi; Inukai, Akira; Kato, Takashi; Liang, Yideng; Kimura, Seigo; Sobue, Gen

doi:10.1007/s00401-002-0635-4

Cited by 103 publications

(55 citation statements)

References 32 publications

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“…27,28 To figure out which factors or molecules in the DMD serum might contribute to miRNA secretion, we investigated the effect of tumor necrosis factor-α (TNF-α), fibroblast growth factor (FGF), and transforming growth factor-β (TGF-β). As shown in Figure 5b , these factors have differential impact on the level of myomiRs in the culture medium of C2C12 myotubes.…”

Section: Resultsmentioning

confidence: 99%

Circulating Muscle-specific miRNAs in Duchenne Muscular Dystrophy Patients

Zhao

et al. 2014

Molecular Therapy - Nucleic Acids

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Noninvasive biomarkers with diagnostic value and prognostic applications have long been desired to replace muscle biopsy for Duchenne muscular dystrophy (DMD) patients. Growing evidence indicates that circulating microRNAs are biomarkers to assess pathophysiological status. Here, we show that the serum levels of six muscle-specific miRNAs (miR-1/206/133/499/208a/208b, also known as myomiRs) were all elevated in DMD patients (P < 0.01). The receiver operating characteristic curves of circulating miR-206, miR-499, miR-208b, and miR-133 levels reflected strong separation between Becker's muscular dystrophy (BMD) and DMD patients (P < 0.05). miR-206, miR-499, and miR-208b levels were positively correlated with both age and type IIc muscle fiber content in DMD patients (2–6 years), indicating that they might represent the stage of disease as well as the process of regeneration. miR-499 and miR-208b levels were correlated with slow and fast fiber content and might reflect the ratio of slow to fast fibers in DMD patient (>6 years). Fibroblast growth factor, transforming growth factor-β, and tumor necrosis factor-α could affect the secretion of myomiRs, suggesting that circulating myomiRs might reflect the effects of cytokines and growth factors on degenerating and regenerating muscles. Collectively, our data indicated that circulating myomiRs could serve as promising biomarkers for DMD diagnosis and disease progression.

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Section: Resultsmentioning

confidence: 99%

Circulating Muscle-specific miRNAs in Duchenne Muscular Dystrophy Patients

Zhao

et al. 2014

Molecular Therapy - Nucleic Acids

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“…DMD patients have higher serum TNF-α levels, and TNF-α-positive fibers have been found by in situ hybridization and immunohistochemistry in muscles of dystrophic DMD subjects (23). Controversial results and muscle type dependent effects have been observed in TNF-α knockout mdx mice; and histopathological analysis has found that the absence of TNF-α in vivo resulted in equivocal findings as opposed to amelioration of muscle pathology as predicted (24), although long-term deletion of TNF-α appeared beneficial in older (12 months) mdx/TNF-α(−/−) mice (25).…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin reduces the expression of myostatin in mdx dystrophic mice

Feder

Rugollini

Santomauro

et al. 2014

Braz J Med Biol Res

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Erythropoietin (EPO) has been well characterized as a renal glycoprotein hormone regulating red blood cell production by inhibiting apoptosis of erythrocyte progenitors in hematopoietic tissues. EPO exerts regulatory effects in cardiac and skeletal muscles. Duchenne muscular dystrophy is a lethal degenerative disorder of skeletal and cardiac muscle. In this study, we tested the possible therapeutic beneficial effect of recombinant EPO (rhEPO) in dystrophic muscles in mdx mice. Total strength was measured using a force transducer coupled to a computer. Gene expression for myostatin, transforming growth factor-β1 (TGF-β1), and tumor necrosis factor-α (TNF-α) was determined by quantitative real time polymerase chain reaction. Myostatin expression was significantly decreased in quadriceps from mdx mice treated with rhEPO (rhEPO=0.60±0.11, control=1.07±0.11). On the other hand, rhEPO had no significant effect on the expression of TGF-β1 (rhEPO=0.95±0.14, control=1.05±0.16) and TNF-α (rhEPO=0.73±0.20, control=1.01±0.09). These results may help to clarify some of the direct actions of EPO on skeletal muscle.

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“…Tumour necrosis factor is a major pro-inflammatory cytokine that is expressed by a wide range of inflammatory cells and by myoblasts, myotubes and damaged skeletal muscle. 25,26 Tumour necrosis factor is also produced by adipose tissue, 27,28 that is often pronounced within the wasted skeletal muscles in DMD. In response to even minor myofibre injury, TNF is rapidly released from resident mast cells and also by neutrophils, which accumulate quickly at sites of tissue damage, 16,29 and TNF is a potent chemokine that attracts further inflammatory cells to the injured site.…”

Section: Role Of Tumour Necrosis Factor In Muscular Dystrophymentioning

confidence: 99%

Implications of Cross‐talk Between Tumour Necrosis Factor and Insulin‐like Growth Factor‐1 Signalling in Skeletal Muscle

Grounds

Radley‐Crabb

Gebski

et al. 2008

Clin Exp Pharma Physio

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1. Inflammation, particularly the pro-inflammatory cytokine tumour necrosis factor (TNF), increases necrosis of skeletal muscle. Depletion of inflammatory cells, such as neutrophils, cromolyn blockade of mast cell degranulation or pharmacological blockade of TNF reduces necrosis of dystrophic myofibres in the mdx mouse model of the lethal childhood disease Duchenne muscular dystrophy (DMD). 2. Insulin-like growth factor-1 (IGF-1) is a very important cytokine for maintenance of skeletal muscle mass and the transgenic overexpression of IGF-1 within muscle cells reduces necrosis of dystrophic myofibres in mdx mice. Thus, IGF-1 usually has the opposite effect to TNF. 3. Activation of TNF signalling via the c-Jun N-terminal kinase (JNK) can inhibit IGF-1 signalling by phosphorylation and conformational changes in insulin receptor substrate (IRS)-1 downstream of the IGF-1 receptor. Such silencing of IGF-1 signalling in situations where inflammatory cytokines are elevated has many implications for skeletal muscle in vivo. 4. The basis for these interactions between TNF and IGF-1 is discussed with specific reference to clinical consequences for myofibre necrosis in DMD and also for the wasting (atrophy) of skeletal muscles that occurs in very old people and in cachexia associated with inflammatory disorders.

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Expression of tumor necrosis factor-α in regenerating muscle fibers in inflammatory and non-inflammatory myopathies

Cited by 103 publications

References 32 publications

Circulating Muscle-specific miRNAs in Duchenne Muscular Dystrophy Patients

Circulating Muscle-specific miRNAs in Duchenne Muscular Dystrophy Patients

Erythropoietin reduces the expression of myostatin in mdx dystrophic mice

Implications of Cross‐talk Between Tumour Necrosis Factor and Insulin‐like Growth Factor‐1 Signalling in Skeletal Muscle

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