Proteomic and bioinformatic analyses of spinal cord injury-induced skeletal muscle atrophy in rats

Wei, Zhijian; Zhou, Xianhu; Fan, Baoyou; Lin, Wei; Ren, Yiming; Feng, Shiqing

doi:10.3892/mmr.2016.5272

Cited by 7 publications

(5 citation statements)

References 78 publications

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“…Importantly, myopenia occurring after SCI is associated with both substantial loss of sub-lesional muscle mass [ 13 , 16 ] and fatty infiltration of muscle [ 16 , 111 ], which together contribute to an obese somatotype [ 112 ], reduced whole-body metabolism [ 113 , 114 ], and increased risk for cardiometabolic disease. [ 112 ] Previous rodent studies of SCI contusion and transection have confirmed changes in sub-lesional muscle size and phenotype, [ 43 , 115 – 117 ] however, these changes have not been evaluated with respect to accompanying consequences. Beyond its notable trophic effects on skeletal muscle, UA reportedly promotes positive outcomes in models of diabetes and hyperlipidemia [ 118 , 119 ], making it an attractive treatment strategy for attenuating secondary health complications associated with cardiometabolic disorders in SCI.…”

Section: Discussionmentioning

confidence: 99%

Effects of ursolic acid on sub-lesional muscle pathology in a contusion model of spinal cord injury

et al. 2018

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Spinal Cord Injury (SCI) results in severe sub-lesional muscle atrophy and fiber type transformation from slow oxidative to fast glycolytic, both contributing to functional deficits and maladaptive metabolic profiles. Therapeutic countermeasures have had limited success and muscle-related pathology remains a clinical priority. mTOR signaling is known to play a critical role in skeletal muscle growth and metabolism, and signal integration of anabolic and catabolic pathways. Recent studies show that the natural compound ursolic acid (UA) enhances mTOR signaling intermediates, independently inhibiting atrophy and inducing hypertrophy. Here, we examine the effects of UA treatment on sub-lesional muscle mTOR signaling, catabolic genes, and functional deficits following severe SCI in mice. We observe that UA treatment significantly attenuates SCI induced decreases in activated forms of mTOR, and signaling intermediates PI3K, AKT, and S6K, and the upregulation of catabolic genes including FOXO1, MAFbx, MURF-1, and PSMD11. In addition, UA treatment improves SCI induced deficits in body and sub-lesional muscle mass, as well as functional outcomes related to muscle function, motor coordination, and strength. These findings provide evidence that UA treatment may be a potential therapeutic strategy to improve muscle-specific pathological consequences of SCI.

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Section: Discussionmentioning

confidence: 99%

Effects of ursolic acid on sub-lesional muscle pathology in a contusion model of spinal cord injury

et al. 2018

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“…Previous studies on muscle atrophy have focused on animal models of disuse atrophy and denervation atrophy; muscle atrophy after SCI is usually classified as either one or a combination of these muscle atrophy models. However, the pathogenesis of muscle atrophy after SCI involves multiple factors, including signal transduction, immunity, electrical conduction, stimulation, and metabolism 20 , 21 . This complex situation cannot be attributed to a single molecular mechanism or simple combinations.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatic analysis of the gene expression profile in muscle atrophy after spinal cord injury

Huang

Xue

Zheng

et al. 2021

Sci Rep

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Spinal cord injury (SCI) is often accompanied by muscle atrophy; however, its underlying mechanisms remain unclear. Here, the molecular mechanisms of muscle atrophy following SCI were investigated. The GSE45550 gene expression profile of control (before SCI) and experimental (14 days following SCI) groups, consisting of Sprague–Dawley rat soleus muscle (n = 6 per group), was downloaded from the Gene Expression Omnibus database, and then differentially expressed gene (DEG) identification and Gene Ontology, pathway, pathway network, and gene signal network analyses were performed. A total of 925 differentially expressed genes, 149 biological processes, and 55 pathways were screened. In the pathway network analysis, the 10 most important pathways were citrate cycle (TCA cycle), pyruvate metabolism, MAPK signalling pathway, fatty acid degradation, propanoate metabolism, apoptosis, focal adhesion, synthesis and degradation of ketone bodies, Wnt signalling, and cancer pathways. In the gene signal network analysis, the 10 most important genes were Acat1, Acadvl, Acaa2, Hadhb, Acss1, Oxct1, Hadha, Hadh, Acaca, and Cpt1b. Thus, we screened the key genes and pathways that may be involved in muscle atrophy after SCI and provided support for finding valuable markers for this disease.

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“…Functional recovery of the animals was evaluated using the Basso Beattie Bresnahan (BBB) locomotor rating scale (17). The BBB was observed by two groups, and the observers were blinded to the design of current experiment (18). The BBB scores of rats were recorded prior to contusion operation and at 1, 3, 5, 7 and 14 days post-injury (dpi).…”

Section: Methodsmentioning

confidence: 99%

Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury

et al. 2019

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Low-frequency pulsed electromagnetic fields (LPEMFs) have been reported to be protective for multiple diseases. However, whether the administration of LPEMFs inhibits inflammation and oxidative stress following spinal cord injury requires further investigation. In the current study, a contusion spinal cord injury model was used and LPEMFs administration was applied to investigate the molecular changes, including inflammation, oxidative stress and heat shock protein 70 (HSP70) levels. The results revealed that LPEMFs significantly promoted functional recovery following spinal cord injury, as demonstrated by an increased Basso, Beattie and Bresnahan score. The results demonstrated that LPEMFs decreased the expression of inflammatory factors, including tumor necrosis factor-α, interleukin-1β and nuclear factor-κB. Additionally, LPEMFs exposure reduced the levels of inducible nitric oxide synthase and reactive oxygen species, and upregulated the expression of catalase and superoxide dismutase. Furthermore, treatment with LPEMFs significantly enhanced the expression of HSP70 in spinal cord-injured rats. Overall, the present study revealed that LPEMFs promote functional recovery following spinal cord injury, potentially by modulating inflammation, oxidative stress and HSP70.

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Proteomic and bioinformatic analyses of spinal cord injury-induced skeletal muscle atrophy in rats

Cited by 7 publications

References 78 publications

Effects of ursolic acid on sub-lesional muscle pathology in a contusion model of spinal cord injury

Effects of ursolic acid on sub-lesional muscle pathology in a contusion model of spinal cord injury

Bioinformatic analysis of the gene expression profile in muscle atrophy after spinal cord injury

Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury

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