Downregulation of ubiquitin-dependent protein degradation in murine myotubes during hyperthermia by eicosapentaenoic acid

Smith, Helen; Khal, Jwan; Tisdale, Michael J.

doi:10.1016/j.bbrc.2005.04.097

Cited by 23 publications

(17 citation statements)

References 19 publications

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“…The beneficial effect of EPA on skeletal muscle wasting is secondary to a decrease in muscle protein degradation by preventing the activation of the ubiquitin-proteasome pathway. This mechanism has been reported in cancer (41), hyperthermia (42), and fasting (48).…”

supporting

confidence: 61%

“…Together these data suggest that EPA decreases the activity of the ubiquitinproteasome pathways induced by chronic inflammation. The inhibitory effect of EPA on skeletal muscle proteolysis can be exerted directly on the muscular cell, since EPA is able to prevent hyperthermia-induced proteolysis by the ubiquitinproteasome in myotube cultures (42).…”

Section: Discussionmentioning

confidence: 99%

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Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

Castillero

Martín

López-Menduiña

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Castillero E, Martín AI, López-Menduiña M, Villanúa MA, López-Calderón A. Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors. Am J Physiol Regul Integr Comp Physiol 297: R1322-R1331, 2009. First published September 9, 2009 doi:10.1152/ajpregu.00388.2009.-Eicosapentaenoic acid (EPA) is an omega-3 polyunsaturated fatty acid that has anti-inflammatory and anticachectic actions. The aim of this work was to elucidate whether EPA administration is able to prevent an arthritis-induced decrease in body weight and muscle wasting in rats. Arthritis was induced by intradermal injection of Freund's adjuvant; 3 days later, nine rats received 1 g/kg EPA or coconut oil daily. All rats were killed 15 days after adjuvant injection. EPA administration decreased the external signs of arthritis and paw volume as well as liver TNF-␣ mRNA. EPA did not modify arthritis-induced decrease in food intake or body weight gain. However, EPA treatment prevented arthritis-induced increase in muscle TNF-␣ and atrogin-1, whereas it attenuated the decrease in gastrocnemius weight and the increase in MuRF1 mRNA. Arthritis not only decreased myogenic regulatory factors but also increased PCNA, MyoD, and myogenin mRNA in the gastrocnemius. Western blot analysis showed that changes in protein content followed the pattern seen with mRNA. In the control rats, EPA administration increased PCNA and MyoD mRNA and protein.In arthritic rats, EPA did not modify the stimulatory effect of arthritis on these myogenic regulatory factors. The results suggest that in experimental arthritis, in addition to its anti-inflammatory effect, EPA treatment attenuates muscle wasting by decreasing atrogin-1 and MuRF1 gene expression and increasing the transcription factors that regulate myogenesis. adjuvant-induced arthritis; ubiquitin-proteasome system; MyoD; myogenin; proliferating cell nuclear antigen CHRONIC INFLAMMATORY DISEASES such as cancer, sepsis, and rheumatoid arthritis are associated with a decrease in body weight, skeletal muscle atrophy, and cachexia. Cachexia is a complex metabolic syndrome associated with underlying

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supporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

Castillero

Martín

López-Menduiña

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This effect may be mediated by the bioavailability of EPA. Moreover, it has been shown in murine models of muscle proteolysis that EPA decreased chymotrypsin-like activity (44,45).…”

Section: Discussionmentioning

confidence: 98%

An α-Linolenic Acid-Rich Formula Reduces Oxidative Stress and Inflammation by Regulating NF-κB in Rats with TNBS-Induced Colitis ,

Hassan¹,

Ibrahim²,

Mbodji³

et al. 2010

The Journal of Nutrition

147

110

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We have previously shown that α-linolenic acid (ALA), a (n-3) PUFA exerts in vitro antiinflammatory effects in the intestine. In this study, we aimed to evaluate its effect on inflammatory and oxidative stress in a colitis model. Colitis was induced in 2 groups at d 0 by intrarectal injection of 2-4-6-trinitrobenzen sulfonic acid (TNBS), whereas the control group received the vehicle. Rats we fed 450 mg . kg(-1) . d(-1) of ALA (TNBS+ALA) while the other colitic group (TNBS) and the control group were fed an isocaloric corn oil formula for 14 d (from d -7 to d 7). RBC fatty acid composition was assessed. Oxidative stress was studied by measuring urinary 8-isoprostanes (8-IP) and colon glutathione (GSH) concentration and inducible nitric oxide synthase (iNOS) expression. Colitis was assessed histologically, by production of proinflammatory mediators, including cytokines, leukotrienes B(4) (LTB(4)), and cyclooxygenase-2 (COX-2) and by nuclear factor-κB (NF-κB) activation. The ALA-rich diet significantly increased the RBC levels of ALA, eicosapentaenoic acid, and docosapentaenoic acid (n-3) compared with the TNBS group (P < 0.01 for all). The beneficial effect of ALA supplementation on oxidative stress was reflected by lower urinary 8-IP levels (P < 0.05), a normalized colon GSH concentration (P < 0.01), and reduced colon iNOS expression (P < 0.05) compared with the TNBS group. ALA also protected against colon inflammation as assessed by lower tumor necrosis factor-α secretion and mRNA level (P < 0.05), reduced NF-κB activation (P = 0.01), and lower colon lipid mediator concentrations such as LTB(4) and COX-2 (P < 0.05) compared with the TNBS group. These findings show that an ALA-rich formula is beneficial to TNBS-induced colitic rats via inhibition of oxidative and inflammatory stress.

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“…Previous studies have shown that increasing the culture temperature from 37˚C to 41˚C results in profound alterations in protein metabolism (22). Our objective was to investigate the protective effect of the cytokine in this particular catabolic condition in murine C2C12 cells submitted to punctual hyperthermia and to study the role of PPAR‰ in mediating IL15 effects (for more details see Materials and methods).…”

Section: Resultsmentioning

confidence: 99%

“…Protein degradation was measured by the release of [2,6-3 H]phenylalanine into the medium after 6-h incubation at 37˚C or 41˚C in the presence of 2 mM cold phenylalanine to prevent reincorporation of the radio-label. The punctual hyperthermia method to induce protein degradation has been previously described by Smith and collaborators (22). Cultures were incubated with or without murine IL15 added at 10 ng/ml in PBS (PeProtech, London, UK) and the PPAR‰ agonist GW501516 at 0.1 μM (Alexis Biochemicals, Lausen, Switzerland) in DMSO:PBS (1:10000).…”

Section: Methodsmentioning

confidence: 99%

PPARδ mediates IL15 metabolic actions in myotubes: Effects of hyperthermia

Fuster

Busquets

Figueras³

et al. 2009

Int J Mol Med

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Abstract. C2C12 cells exposed to hyperthermia (41˚C) experienced an increase in both protein synthesis and degradation. The addition of IL15 under hyperthermic conditions resulted in an important increase in protein synthesis with no changes in protein degradation, except when cells overexpressed PPAR‰. The PPAR‰ agonist GW501516 exerted similar effects on protein synthesis to IL15. Expression of a mutant dominant negative form of PPAR‰ prevented the effect of the cytokine on protein synthesis, suggesting that this transcription factor is involved in the anabolic action of IL15. The present study also suggests that the effects of IL15 on lipid oxidation could be mediated by PPAR‰.

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Downregulation of ubiquitin-dependent protein degradation in murine myotubes during hyperthermia by eicosapentaenoic acid

Cited by 23 publications

References 19 publications

Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

An α-Linolenic Acid-Rich Formula Reduces Oxidative Stress and Inflammation by Regulating NF-κB in Rats with TNBS-Induced Colitis ,

PPARδ mediates IL15 metabolic actions in myotubes: Effects of hyperthermia

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