Total and myofibrillar protein breakdown in different types of rat skeletal muscle: Effects of sepsis and regulation by insulin

Hasselgren, Per-Olof; James, J. Howard; Benson, D. W.; Hall-Angerås, Marianne; Angerås, Ulf; Hiyama, Darryl T.; Li, Shujun; Fischer, Josef E.

doi:10.1016/0026-0495(89)90100-5

Cited by 145 publications

(110 citation statements)

References 24 publications

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“…In addition to muscle damage and increased inflammatory signaling, it is also thought that increases in protein degradation 41 It is thought that protein degradation is controlled, at least in part, by the activity of the muscle E3 ligases, MURF-1 and MAFbx, which, in turn, are thought to be regulated by FOXO-1. The activity of FOXO-1 is controlled by its phosphorylation by Akt, with increased FOXO-1 phosphorylation causing a decrease in its transcriptional activity.…”

Section: Ceo 2 Nanoparticle Treatment Improves Protein Degradation/ Smentioning

confidence: 99%

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

Asano¹,

Arvapalli²,

Manne³

et al. 2015

IJN

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The severe inflammation observed during sepsis is thought to cause diaphragm dysfunction, which is associated with poor patient prognosis. Cerium oxide (CeO 2 ) nanoparticles have been posited to exhibit anti-inflammatory and antioxidative activities suggesting that these particles may be of potential use for the treatment of inflammatory disorders. To investigate this possibility, Sprague Dawley rats were randomly assigned to the following groups: sham control, CeO 2 nanoparticle treatment only (0.5 mg/kg iv), sepsis, and sepsis+CeO 2 nanoparticles. Sepsis was induced by the introduction of cecal material (600 mg/kg) directly into the peritoneal cavity. Nanoparticle treatment decreased sepsis-associated impairments in diaphragmatic contractile ( P o ) function (sham: 25.6±1.6 N/cm 2 vs CeO 2 : 23.4±0.8 N/cm 2 vs Sep: 15.9±1.0 N/cm 2 vs Sep+CeO 2 : 20.0±1.0 N/cm 2 , P <0.05). These improvements in diaphragm contractile function were accompanied by a normalization of protein translation signaling (Akt, FOXO-1, and 4EBP1), diminished proteolysis (caspase 8 and ubiquitin levels), and decreased inflammatory signaling (Stat3 and iNOS). Histological analysis suggested that nanoparticle treatment was associated with diminished sarcolemma damage and diminished inflammatory cell infiltration. These data indicate CeO 2 nanoparticles may improve diaphragmatic function in the septic laboratory rat.

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Section: Ceo 2 Nanoparticle Treatment Improves Protein Degradation/ Smentioning

confidence: 99%

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

Asano¹,

Arvapalli²,

Manne³

et al. 2015

IJN

View full text Add to dashboard Cite

show abstract

“…Many studies have provided evidence that muscle atrophy in sepsis is primarily the result of increased protein breakdown [Hasselgren et al, 1986[Hasselgren et al, , 1989Ash and Griffin, 1989] via the ubiquitinproteasome pathway [Tiao et al, 1994[Tiao et al, , 1997. Indeed, both atrogin-1/MAFbx and MuRF1 are upregulated in the muscle of septic models induced by either cecal ligation and puncture [Wray et al, 2003] or lipopolysaccharide (LPS) administration [Dehoux et al, 2003].…”

Section: Introductionmentioning

confidence: 99%

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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“…The increased protein breakdown seems to play a major role in muscle wasting as observed in rats with sepsis (Hasselgren et al 1989) and in cancer patients (Tisdale 2000). Skeletal muscle contains three major proteolytic systems; one of them is the ubiquitin-proteasome-dependent pathway that mediates the degradation of the most abundant contractile proteins (Mitch & Goldberg 1996).…”

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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Chronic inflammation is associated with a decrease in body weight and cachexia, which is characterized by anorexia and skeletal muscle wasting. The expression of atrogens muscle RING finger-1 (MuRF-1) and muscle atrophy F-box (MAFbx) are increased in muscle atrophy and it is known that tumour necrosis factor (TNF) regulates skeletal muscle loss through TNF receptor p55 (TNFRI). The aim of this study was to examine the effect of polyethylene glycol linked to soluble TNFRI (PEG-sTNFRI) on gene expression of the atrogens MuRF-1 and MAFbx in skeletal muscle of arthritic rats. Rats were injected with Freund's adjuvant and, 15 days later, arthritic and control rats were injected daily with PEG-sTNFRI (1 mg/kg, s.c.) or saline for 8 days. Arthritis decreased body weight gain, the weight of skeletal muscle and adipose mass. PEG-sTNFRI administration increased body weight gain and adipose mass of arthritic rats; however, it did not modify the skeletal muscle weight. The gene expression of TNF-a, MuRF1 and MAFbx, IGF-I and IGFBP-5 were increased in the skeletal muscle of arthritic rats, and the administration of PEG-sTNFRI did not modify these parameters. These data suggest that the anti-TNF agent PEG-sTNFRI did not prevent the increase in E3 ubiquitinligating enzymes, MuRF1 and MAFbx, gene expression in the skeletal muscle of arthritic rats.

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Total and myofibrillar protein breakdown in different types of rat skeletal muscle: Effects of sepsis and regulation by insulin

Cited by 145 publications

References 24 publications

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

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

Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats

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