Proteomic and bioinformatic analysis of differentially expressed proteins in denervated skeletal muscle

Sun, Hualin; Qiu, Jiaying; Chen, Yanfei; Yu, Miaomei; Ding, Fei; Gu, Xiaosong

doi:10.3892/ijmm.2014.1737

Cited by 28 publications

(24 citation statements)

References 42 publications

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“…Cell culture was performed as described previously [8,23]. Briefly, C2C12 cells were obtained from the Cell Bank at the Chinese Academy of Sciences (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

TRAF6 Inhibition Rescues Dexamethasone-Induced Muscle Atrophy

Sun

Gong

Qiu

et al. 2014

IJMS

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Tumor necrosis factor receptor-associated factor 6 (TRAF6), a unique E3 ubiquitin ligase and adaptor protein, is involved in activation of various signaling cascades. Recent studies identify TRAF6 as one of the novel regulators of skeletal muscle atrophy. The role of TRAF6 in glucocorticoid-induced muscle atrophy, however, remains to be elucidated. In this study, we show that TRAF6 and its downstream signaling molecules, muscle atrophy F-box (MAFBx) and muscle ring finger 1 (MuRF1), were all upregulated in dexamethasone-induced atrophy of mouse C2C12 myotubes or mouse tibialis anterior (TA) muscle. To further investigate the role of TRAF6 in dexamethasone-induced muscle atrophy, TRAF6-siRNA was used to transfect cultured C2C12 myotubes or was injected into the TA muscle of mice respectively, and we note that TRAF6 knockdown attenuated dexamethasone-induced muscle atrophy in vitro and in vivo, and concomitantly decreased the expression of MuRF1 and MAFBx. Our findings suggest that a decreased expression of TRAF6 could rescue dexamethasone-induced skeletal muscle atrophy through, at least in part, regulation of the expression of MAFBx and MuRF1.

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“…Cell culture was performed as described previously [8,23]. Briefly, C2C12 cells were obtained from the Cell Bank at the Chinese Academy of Sciences (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

TRAF6 Inhibition Rescues Dexamethasone-Induced Muscle Atrophy

Sun

Gong

Qiu

et al. 2014

IJMS

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“…Previous studies have been concerned with denervation-induced skeletal muscle atrophy following peripheral nerve injury (4,5). Therefore, isobaric tags for relative and absolute quantification coupled with two-dimensional liquid chromatography-tandem mass spectrometry were performed in order to identify the differentially expressed proteins in the tibialis anterior (TA) muscle 1 and 4 weeks following sciatic nerve transection in rats (4).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, isobaric tags for relative and absolute quantification coupled with two-dimensional liquid chromatography-tandem mass spectrometry were performed in order to identify the differentially expressed proteins in the tibialis anterior (TA) muscle 1 and 4 weeks following sciatic nerve transection in rats (4). The results demonstrated that tumor necrosis factor receptor-associated factor 6 (TRAF6) was upregulated in denervated TA muscle (4). Conversely, the results also demonstrated that knockdown of TRAF6 significantly attenuated glucocorticoid-induced myotube atrophy in vitro and in vivo (5).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

Qiu

Dai

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) have been observed to be involved in the modulation of various physiopathological processes. However, the impacts of miRNAs on muscle atrophy have not been fully investigated. In the present study, the results demonstrated that miR-351 was differentially expressed in the tibialis anterior (TA) muscle at various times following sciatic nerve transection, and the time-dependent expression profile of miR-351 was inversely correlated with that of tumor necrosis factor receptor-associated factor 6 (TRAF6) at the mRNA and protein levels. The dual luciferase reporter assay indicated that miR-351 was able to significantly downregulate the expression levels of TRAF6 by directly targeting the 3'-untranslated region of TRAF6. Overexpression of miR-351 inhibited a significant decrease in the wet weight ratio or cross-sectional area of the TA muscle following sciatic nerve transection. Western blot analysis indicated that the protein expression levels of TRAF6, muscle ring-finger protein 1 (MuRF1) and muscle atrophy F-box (MAFBx) in denervated TA muscles were suppressed by overexpression of miR-351. These results demonstrate that miR-351 inhibits denervation-induced atrophy of TA muscles following sciatic nerve transection at least partially through negative regulation of TRAF6 as well as MuRF1 and MAFBx, the two downstream signaling molecules of TRAF6.

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“…Ten randomly selected fields were observed using an inverted microscope (Olympus Corporation, Tokyo, Japan) and the transaction diameter values of all four groups were measured prior to cell harvesting, as previously described (16). …”

Section: Methodsmentioning

confidence: 99%

Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway

Geng

Wei

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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The present study aimed to determine the effect of Astragalus polysaccharide (APS) in an in vivo and in vitro rat model of muscle atrophy (cachexia) caused by chronic renal failure (CRF), along with the potential corresponding roles of atroglin-1 and the ubiquitin-proteasome pathway. A rat model of CRF was established using subtotal bilateral nephrectomy. It was observed by reverse transcription-quantitative polymerase chain reaction and western blot analysis that APS and the specific inhibitor of nuclear factor (NF)-κB, pyrrolidine dithiocarbamate (PDTC), significantly reduced the expression of atrogin-1, ubiquitin and the NF-κB subunit p65 mRNA in rat skeletal muscle in vivo and in vitro, respectively (P<0.05). NF-κB and PDTC also markedly reduced the expression of atrogin-1, ubiquitin and p65 protein. In addition, cultured rat myoblasts pretreated with tumor necrosis factor (TNF)-α exhibited significantly reduced expression of atrogin-1, ubiquitin and p65 mRNA in vitro (P<0.05). Fluorescence microscopy was subsequently used to evaluate TNF-α-treated myoblasts administered with APS or PDTC, whereby no evidence of muscle cell atrophy was observed in cells treated with APS. These data suggest that APS may delay muscle cell atrophy associated with cachexia in CRF by targeting atrogin-1 and the ubiquitin-proteasome pathway.

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Proteomic and bioinformatic analysis of differentially expressed proteins in denervated skeletal muscle

Cited by 28 publications

References 42 publications

TRAF6 Inhibition Rescues Dexamethasone-Induced Muscle Atrophy

TRAF6 Inhibition Rescues Dexamethasone-Induced Muscle Atrophy

MicroRNA-351 inhibits denervation-induced muscle atrophy by targeting TRAF6

Astragalus polysaccharide, a component of traditional Chinese medicine, inhibits muscle cell atrophy (cachexia) in an in vivo and in vitro rat model of chronic renal failure by activating the ubiquitin-proteasome pathway

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