The analysis of antioxidant expression during muscle atrophy induced by hindlimb suspension in mice

Nuoc, Tran-Non; Kim, Suhee; Ahn, Sun Hee; Lee, Jin-Sil; Park, Byung-Ju; Lee, Tae‐Hoon

doi:10.1007/s12576-016-0444-5

Cited by 18 publications

(14 citation statements)

References 28 publications

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“…Additionally, we identified the up-regulated transcripts Ddit4 and Eif4ebp1 ( Figure 3A), which have been previously implicated in protein synthesis during skeletal muscle atrophy [29,30]. We also found upregulation in the expression of the antioxidant genes Gpx3, Mt1, and Mt2 ( Figure 3A), which have been described with a role in muscle repair in atrophic conditions [31][32][33].…”

Section: Relevant Transcripts and Regulatory Pathways Associated Withsupporting

confidence: 52%

MicroRNA-mRNA Co-sequencing Identifies Transcriptional and Post-transcriptional Regulatory Networks Underlying Muscle Wasting in Cancer Cachexia

Fernández¹,

Ferreira²,

Vechetti³

et al. 2019

Preprint

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Cachexia is a complex metabolic syndrome characterized by loss of skeletal muscle, leading to a significant weight loss that impacts patient morbidity and mortality. Given the complexity of gene regulatory networks that control gene expression, our objective was to perform an integrative mRNA and miRNA profiling to identify genetic programs that capture essential mechanistic details that promote muscle atrophy in cancer cachexia. Here, we used RNA sequencing to analyze miRNAs and mRNAs expression profiles in tibialis anterior (TA) muscles of the Lewis lung carcinoma model of cancer cachexia. In addition, we compared these findings with RNA-Seq data from C2C12 myotubes treated in vitro with the cachectic factors tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). Extracellular matrix (ECM) alterations were validated by picrosirius staining, western blot, and fractal dimension analyses. We found 1,008 mRNAs and 18 miRNAs differentially expressed in cachectic mice. This set of genes was associated with the ECM, proteolysis, and inflammatory response. Enrichment analysis of transcriptional factor binding sites revealed activation of the atrophy-related transcriptional factors: NF-κB, Stat3, AP-1, and FoxO. Furthermore, the integration of mRNA and miRNA expression profiles identified posttranscriptional regulation by miRNAs of genes involved in ECM organization, cell migration, transcription factors binding, ion transport, and FoxO signaling pathway. C2C12 myotubes treated with TNF-α and IFN-γ similarly down-regulate subsets of ECM genes, including collagens. Our integrative analysis of miRNA-mRNA co-profiles comprehensive characterized regulatory relationships of molecular pathways and revealed miRNAs targeting ECM-associated genes in cancer cachexia. We also confirmed in C2C12 myotubes that changes in ECM-associated genes are dependent on inflammatory signaling of the cytokines TNF-α and IFN-γ.

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Section: Relevant Transcripts and Regulatory Pathways Associated Withsupporting

confidence: 52%

MicroRNA-mRNA Co-sequencing Identifies Transcriptional and Post-transcriptional Regulatory Networks Underlying Muscle Wasting in Cancer Cachexia

Fernández¹,

Ferreira²,

Vechetti³

et al. 2019

Preprint

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“…ROS generating subunits (Nox1) were significantly elevated indicating ROS is increased during atrophy. Also, a decrease in the expression of antioxidants that scavenge ROS and a decrease in subunits of the mitochondrial complex 1 were observed, further indicating mitochondrial dysfunction associated with atrophy (Nuoc et al, 2016).…”

Section: Mitochondrial Dysfunction Associated With Atrophymentioning

confidence: 97%

The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy

Theilen

Kunkel

Tyagi

2017

Journal Cellular Physiology

117

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Skeletal muscle atrophy is the consequence of protein degradation exceeding protein synthesis. This arises for a multitude of reasons including the unloading of muscle during microgravity, post-surgery bedrest, immobilization of a limb after injury, and overall disuse of the musculature. The development of therapies prior to skeletal muscle atrophy settings to diminish protein degradation is scarce. Mitochondrial dysfunction is associated with skeletal muscle atrophy and contributes to the induction of protein degradation and cell apoptosis through increased levels of ROS observed with the loss of organelle function. ROS binds mtDNA, leading to its degradation and decreasing functionality. Mitochondrial transcription factor A (TFAM) will bind and coat mtDNA, protecting it from ROS and degradation while increasing mitochondrial function. Exercise stimulates cell signaling pathways that converge on and increase PGC-1α, a well-known activator of the transcription of TFAM and mitochondrial biogenesis. Therefore, in the present review we are proposing, separately, exercise and TFAM treatments prior to atrophic settings (muscle unloading or disuse) alleviate skeletal muscle atrophy through enhanced mitochondrial adaptations and function. Additionally, we hypothesize the combination of exercise and TFAM leads to a synergistic effect in targeting mitochondrial function to prevent skeletal muscle atrophy.

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“…Although there were no changes in elevated levels of non-heme iron, oxidative damage was decreased after reloading for seven and 14 days [ 112 ]. Mice were subjected to HLU for two weeks; the results suggested that imbalanced redox homeostasis occurred during muscle atrophy, due to the activation of NOX1, the deficiency of mitochondrial complex I, and the interference of antioxidants [ 113 ]. It has been well demonstrated that reduced protein synthesis and elevated protein degradation in muscle seems to be the major trigger in disuse muscle atrophy.…”

Section: Iron and Ros Signaling In Spaceflight-induced-bone Loss Amentioning

confidence: 99%

Effects of Iron Overload and Oxidative Damage on the Musculoskeletal System in the Space Environment: Data from Spaceflights and Ground-Based Simulation Models

Yang

Zhang

Dong

et al. 2018

IJMS

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The space environment chiefly includes microgravity and radiation, which seriously threatens the health of astronauts. Bone loss and muscle atrophy are the two most significant changes in mammals after long-term residency in space. In this review, we summarized current understanding of the effects of microgravity and radiation on the musculoskeletal system and discussed the corresponding mechanisms that are related to iron overload and oxidative damage. Furthermore, we enumerated some countermeasures that have a therapeutic potential for bone loss and muscle atrophy through using iron chelators and antioxidants. Future studies for better understanding the mechanism of iron and redox homeostasis imbalance induced by the space environment and developing the countermeasures against iron overload and oxidative damage consequently may facilitate human to travel more safely in space.

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The analysis of antioxidant expression during muscle atrophy induced by hindlimb suspension in mice

Cited by 18 publications

References 28 publications

MicroRNA-mRNA Co-sequencing Identifies Transcriptional and Post-transcriptional Regulatory Networks Underlying Muscle Wasting in Cancer Cachexia

MicroRNA-mRNA Co-sequencing Identifies Transcriptional and Post-transcriptional Regulatory Networks Underlying Muscle Wasting in Cancer Cachexia

The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy

Effects of Iron Overload and Oxidative Damage on the Musculoskeletal System in the Space Environment: Data from Spaceflights and Ground-Based Simulation Models

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