Role of miRNAs and lncRNAs in dexamethasone‑induced myotube atrophy <i>in vitro</i>

Yang, Li; Shi, Huacai; Chen, Rui; Zhou, Shanyao; Liu, Si; She, Yanling

doi:10.3892/etm.2020.9577

Cited by 6 publications

(2 citation statements)

References 67 publications

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“…Among them, the expression of 1110038B12Rik was robustly increased under these cachexia conditions; therefore, 1110038B12Rik was named Atrolnc-1 . Increased Atrolnc-1 expression after fasting was confirmed and observed after dexamethasone treatment in mice [ 92 , 93 ]. Overexpression and knockdown of Atrolnc-1 in C2C12 myotubes revealed that Atrolnc-1 promoted proteolysis without affecting protein synthesis.…”

Section: Lncrnas Related To Muscle Atrophy and Hypertrophy Conditionsmentioning

confidence: 94%

The Functional Role of Long Non-Coding RNA in Myogenesis and Skeletal Muscle Atrophy

Hitachi

Honda

Tsuchida

2022

Cells

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Skeletal muscle is a pivotal organ in humans that maintains locomotion and homeostasis. Muscle atrophy caused by sarcopenia and cachexia, which results in reduced muscle mass and impaired skeletal muscle function, is a serious health condition that decreases life longevity in humans. Recent studies have revealed the molecular mechanisms by which long non-coding RNAs (lncRNAs) regulate skeletal muscle mass and function through transcriptional regulation, fiber-type switching, and skeletal muscle cell proliferation. In addition, lncRNAs function as natural inhibitors of microRNAs and induce muscle hypertrophy or atrophy. Intriguingly, muscle atrophy modifies the expression of thousands of lncRNAs. Therefore, although their exact functions have not yet been fully elucidated, various novel lncRNAs associated with muscle atrophy have been identified. Here, we comprehensively review recent knowledge on the regulatory roles of lncRNAs in skeletal muscle atrophy. In addition, we discuss the issues and possibilities of targeting lncRNAs as a treatment for skeletal muscle atrophy and muscle wasting disorders in humans.

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Section: Lncrnas Related To Muscle Atrophy and Hypertrophy Conditionsmentioning

confidence: 94%

The Functional Role of Long Non-Coding RNA in Myogenesis and Skeletal Muscle Atrophy

Hitachi

Honda

Tsuchida

2022

Cells

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“…Glucocorticoids, which have anti-inflammatory and immune-suppressing properties, are commonly used in the treatment of several diseases, such as rheumatoid arthritis, systemic lupus erythematosus, bronchial asthma, adult dyspnea syndromes, autoimmune diseases, and others [ 4 , 5 , 6 ]. However, high doses or prolonged use of these drugs can cause many side effects including muscle weakness and atrophy [ 7 , 8 ]. Chronic or excessive exposure to glucocorticoids induces muscle atrophy through ubiquitin-proteasome and lysosomal pathways.…”

Section: Introductionmentioning

confidence: 99%

Morpho-Functional Analyses Demonstrate That Tyrosol Rescues Dexamethasone-Induced Muscle Atrophy

Salucci,

Burattini,

Versari

et al. 2024

JFMK

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Prolonged exposure to high dosages of dexamethasone, which is a synthetic glucocorticoid and a well-known anti-inflammatory drug, may lead to an increase in reactive oxygen species production, contributing to muscle wasting. The prevention of muscle atrophy by ingestion of functional foods is an attractive issue. In the last decade, natural antioxidant compounds have been increasingly investigated as promising molecules able to counteract oxidative-stress-induced muscle atrophy. Recently, we have demonstrated the antioxidant properties of two main olive oil polyphenols also known for their anticancer and anti-inflammatory activities in different cell models. Here, the preventive effect of tyrosol on dexamethasone-induced muscle atrophy has been investigated by means of morpho-functional approaches in C2C12 myotubes. Dexamethasone-treated cells showed a reduced fiber size when compared to control ones. While long and confluent myotubes could be observed in control samples, those exposed to dexamethasone appeared as immature syncytia. Dysfunctional mitochondria and the accumulation of autophagic vacuoles contributed to myotube degeneration and death. Tyrosol administration before glucocorticoid treatment prevented muscle wasting and rescued mitochondrial and lysosomal functionality. These findings demonstrate that tyrosol attenuates dexamethasone-induced myotube damage, and encourage the use of this natural molecule in preclinical and clinical studies and in synergy with other functional foods or physical activity with the aim to prevent muscle atrophy.

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Circulating myomiRNAs as biomarkers in patients with Cushing’s syndrome

Pivonello,

Patalano,

Simeoli

et al. 2023

J Endocrinol Invest

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Purpose Impairment of skeletal muscle mass and strength affects 40–70% of patients with active Cushing’s syndrome (CS). Glucocorticoid excess sustains muscle atrophy and weakness, while muscle-specific microRNAs (myomiRs) level changes were associated with muscle organization and function perturbation. The aim of the current study is to explore changes in circulating myomiRs in CS patients compared to healthy controls and their involvement in IGFI/PI3K/Akt/mTOR pathway regulation in skeletal muscle. Methods C2C12, mouse myocytes, were exposed to hydrocortisone (HC), and atrophy-related gene expression was investigated by RT-qPCR, WB and IF to assess HC-mediated atrophic signalling. miRNAs were evaluated in HC-treated C2C12 by PCR Arrays. MyomiRs significantly overexpressed in C2C12 were investigated in 37 CS patients and 24 healthy controls serum by RT-qPCR. The anti-anabolic role of circulating miRNAs significantly upregulated in CS patients was explored in C2C12 by investigating the IGFI/PI3K/Akt/mTOR pathway regulation. Results HC induced higher expression of atrophy-related genes, miR-133a-3p, miR-122-5p and miR-200b-3p in C2C12 compared to untreated cells. Conversely, the anabolic IGFI/PI3K/Akt/mTOR signalling was reduced and this effect was mediated by miR-133a-3p. In CS patients miR-133a-3p and miR-200b-3p revealed higher circulating levels (p < 0.0001, respectively) compared to controls. ROC curves for miR-133a-3p (AUC 0.823, p < 0.0001) and miR-200b-3p (AUC 0.850, p < 0.0001) demonstrated that both myomiRs represent potential biomarkers to discriminate between CS and healthy subjects. Pearson’s correlation analysis revealed that circulating levels of miR-133a-3p are directly correlated with 24 h urinary-free cortisol level (r = 0.468, p = 0.004) in CS patients. Conclusions HC induces atrophic signals by miR-133a-3p overexpression in mouse myocytes and humans. Circulating miR-133a-3p is promising biomarkers of hypercortisolism.

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Role of miRNAs and lncRNAs in dexamethasone‑induced myotube atrophy in vitro

Cited by 6 publications

References 67 publications

The Functional Role of Long Non-Coding RNA in Myogenesis and Skeletal Muscle Atrophy

The Functional Role of Long Non-Coding RNA in Myogenesis and Skeletal Muscle Atrophy

Morpho-Functional Analyses Demonstrate That Tyrosol Rescues Dexamethasone-Induced Muscle Atrophy

Circulating myomiRNAs as biomarkers in patients with Cushing’s syndrome

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