Cytokines and oxidative signalling in skeletal muscle

Reid, Michael B.; Li, Yi-Ping

doi:10.1046/j.1365-201x.2001.00824.x

Cited by 165 publications

(115 citation statements)

References 85 publications

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“…Reactive oxygen species (ROS) is implicated in muscle wasting, and LPS is known to induce oxidative stress [Reid and Li, 2001]. However, our finding that activation of the redoxsensitive transcription factor NF-κB [Li et al, 1999] by LPS in muscle is not affected by curcumin suggests that curcumin does not inhibit atrogin-1/MAFbx upregulation by functioning as a general antioxidant.…”

Section: Discussioncontrasting

confidence: 52%

Curcumin prevents lipopolysaccharide‐induced atrogin‐1/MAFbx upregulation and muscle mass loss

Jin

2006

J of Cellular Biochemistry

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Because elevated ubiquitin ligase atrogin-1/MAFbx and MuRF1 mediate skeletal muscle wasting associated with various catabolic conditions, the signaling pathways involved in the upregulation of these genes under pathological conditions are considered therapeutic targets. AKT and NF-κB have been previously shown to regulate the expression of atrogin-1/MAFbx or MuRF1, respectively. In addition, we recently found that p38 MAPK mediates TNF-α upregulation of atrogin-1/MAFbx expression, suggesting that multiple signaling pathways mediate muscle wasting in inflammatory diseases. To date, however, these advances have not resulted in a practical clinical intervention for disease-induced muscle wasting. In the present study, we tested the effect of curcumin-a non-toxic anti-inflammatory reagent that inhibits p38 and NF-κB-on lipopolysaccharide (LPS)-induced muscle wasting in mice. Daily intraperitoneal (i.p.) injection of curcumin (10-60 μg/kg) for 4 days inhibited, in a dose-dependent manner, the LPS-stimulated (1 mg/kg, i.p.) increase of atrogin-1/MAFbx expression in gastrocnemius and extensor digitorum longus (EDL) muscles, resulting in the attenuation of muscle protein loss. It should also be noted that curcumin administration did not alter the basal expression of atrogin-1/MAFbx, nor did it affect LPS-stimulated MuRF1 and polyubiquitin expression. LPS activated p38 and NF-κB, while inhibiting AKT; whereas, curcumin administration inhibited LPS-stimulated p38 activation, without altering the effect of LPS on NF-κB and AKT. These results indicate that curcumin is effective in blocking LPS-induced loss of muscle mass through the inhibition of p38-mediated upregulation of atrogin-1/MAFbx. Keywords endotoxemia; ubiquitin-proteasome pathway; p38; AKT; NF-κB Muscle wasting is a major feature of the cachexia associated with such diseases as sepsis, cancer, AIDS, diabetes, uremia, congestive heart failure, and chronic obstructive pulmonary disease (COPD) [Hasselgren, 1995;Tisdale, 1997]. Muscle wasting increases patient morbidity and mortality through disability, injury, osteoporosis, impairment of respiratory function, and depletion of the free amino acid pool for enzyme and antibody production. The progressive loss of body protein becomes lethal when it depletes approximately 40% of lean body mass [Winick, 1979]. However, to date, no drug has been approved for muscle wasting. Muscle wasting is primarily caused by accelerated muscle protein breakdown via the ubiquitin-proteasome pathway . Proteins degraded by this pathway are first covalently linked to a chain of ubiquitin molecules that marks them for rapid breakdown by the 26S proteasome. The selectivity of ubiquitin targeting is primarily a function of ubiquitin ligase (E3 protein) [Hershko and Ciechanover, 1998]. Two muscleenriched ubiquitin ligases, atrogin-1/MAFbx and MuRF1, are rate limiting for muscle protein loss in various catabolic conditions. Expression of these two ubiquitin ligases is upregulated in the muscle of various animal models of muscle atrophy,...

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Section: Discussioncontrasting

confidence: 52%

Curcumin prevents lipopolysaccharide‐induced atrogin‐1/MAFbx upregulation and muscle mass loss

Jin

2006

J of Cellular Biochemistry

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“…Muscle strenuous contraction induces protein loss and cachexia (25). However, we found no evidence to support respiratory muscle overloading (as discussed above), which could lead to increased expression of muscle cytokines.…”

Section: The Experimental Modelcontrasting

confidence: 50%

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Tarasiuk¹,

Segev²

2007

Journal of Applied Physiology

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Tarasiuk A, Segev Y. Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats. J Appl Physiol 102: [913][914][915][916][917][918] 2007. First published November 30, 2006; doi:10.1152/japplphysiol.00838.2006.-The effect of upper airway loading on longitudinal bone growth and various components of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis has not been fully elucidated. In the present study, the effect of chronic resistive airway loading (CAL) in a prepubescent rat model on linear bone growth and weight gain was investigated. We hypothesize that CAL induced in prepubescent rats will lead to impaired longitudinal growth due to impairment in circulating and liver GH/IGF-I parameters. The tracheae of 22-day-old rats were obstructed by tracheal banding to increase inspiratory esophageal pressure. The GH/IGF-I markers were analyzed using ELISA, RT-PCR, and Western immunoblot analysis 14 days after surgery. Animals exhibited impaired longitudinal growth as demonstrated by reduction of tibia and tail length gains by 40% (P Ͻ 0.0001) and body weight gain by 24% (P Ͻ 0.0001). No differences were seen in total body energy balance, i.e., oxygen consumption, daily food intake, or arterial blood gases. Circulating GH, IGF-I, and IGF binding protein-3 (IGFBP-3) levels were reduced by 40% (P ϭ 0.037), 30% (P Ͻ 0.006), and 27% (P ϭ 0.02), respectively, in the CAL group. Liver IGF-I mRNA level decreased by 20% (P Ͻ 0.0002), whereas GH receptor mRNA and protein expression were unchanged. We conclude that impaired longitudinal growth in prepubescent CAL rats is related to a decrease in GH, IGF-I, and IGFBP-3 levels. chronic resistive loading; growth hormone; insulin-like growth factor I; insulin-like growth factor binding protein-3; prepuberty ONE OF THE CONSEQUENCES OF chronic resistive airway loading (CAL) in adult rats is malfunction in body weight gain (12, 27) without effect on longitudinal bone growth (35). The failure to gain weight was not related to decreased caloric intake (12) and was recently attributed to a decline in serum insulin-like growth factor I (IGF-I) levels (35). The endocrine effect of pituitary-secreted growth hormone (GH) is induction of IGF-I and IGF binding protein-3 (IGFBP-3) synthesis in various organs, including the liver; both are highly correlated with the 24-h mean GH levels (3, 7). This effect is mediated via activation of GH receptor (GHR), which is extensively distributed throughout many tissues (9). Impairment of the GH/IGF-I axis in prepubescent rats, before bone growth is completed, leads to skeletal growth retardation (31). The effect of CAL on the GH/IGF-I axis and longitudinal growth in prepuberty rats is not known.In the present study, the effect of CAL on longitudinal growth and weight gain was studied using the prepubescent rat model. We hypothesize that CAL will impair the GH/IGF-I axis, consequently leading to longitudinal growth retardation. We explored the effect of CAL on linear growth, serum GH, IGF-I, and ...

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“…Since TNFα can also stimulate the production of mitochondrial ROS, 62 this could create a positive feedback loop whereby the increased ROS cause further activation of NF-κBa s well as having their own deleterious effects on the muscle. 38 This idea is supported by a recent paper which reported that mdx mice injected with an anti-TNFα antibody,R emicade, displayed less muscle necrosis and reduced inflammatory cell infiltration than control mdx mice.…”

Section: Rosand Inflammatory Damage Ofdystrophic Musclementioning

confidence: 99%

MUSCLE DAMAGE IN MDX (DYSTROPHIC) MICE: ROLE OF CALCIUM AND REACTIVE OXYGEN SPECIES

Whitehead

Yeung

Allen

2006

Clin Exp Pharma Physio

269

234

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SUMMARY Duchenne muscular dystrophy (DMD) is a lethal, degenerative muscle disease caused by a genetic mutation that leads to the complete absence of the cytoskeletal protein dystrophin in muscle fibres. The present review provides an overview of some of the physiological pathways that may contribute to muscle damage and degeneration in DMD, based primarily on experimental findings in the mdx mouse, an animal model of this disease. A rise in intracellular calcium is widely thought to be an important initiating event in the dystrophic pathogenesis. The pathway(s) leading to increased intracellular calcium in dystrophin deficient muscle is uncertain, but recent work from our laboratory provides evidence that stretch‐activated channels are an important source of the calcium influx. Other possible routes of calcium entry are also discussed. The consequences of elevated cytosolic calcium may include activation of proteases, such as calpain, and increased production of reactive oxygen species (ROS), which can cause protein and membrane damage. Another possible cause of damage in dystrophic muscle involves inflammatory pathways, such as those mediated by neutrophils, macrophages and associated cytokines. There is recent evidence that increased ROS may be important in both the activation of and the damage caused by this inflammatory pathway in mdx muscle.

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Cytokines and oxidative signalling in skeletal muscle

Cited by 165 publications

References 85 publications

Curcumin prevents lipopolysaccharide‐induced atrogin‐1/MAFbx upregulation and muscle mass loss

Curcumin prevents lipopolysaccharide‐induced atrogin‐1/MAFbx upregulation and muscle mass loss

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

MUSCLE DAMAGE IN MDX (DYSTROPHIC) MICE: ROLE OF CALCIUM AND REACTIVE OXYGEN SPECIES

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