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Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE227496 | GEO | 2023/03/21

REPOSITORIES: GEO

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Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction [C2C12]

Project description:Jakyak-gamcho-tang (JGT) is a herbal medicine that has been traditionally prescrived for pain control including muscular pain. This transcriptome analysis aims to investigate the changes in global gene expression profile in differentiated murine C2C12 myotube cells treated with JGT extract.

2023-03-21 | GSE227494 | GEO

Jakyak-gamcho-tang ameliorates dexamethasone (DEX)-induced muscle atrophy and muscle dysfunction [Gastrocnemius and Soleus]

Project description:Jakyak-gamcho-tang (JGT) is a herbal medicine that has been traditionally prescrived for pain control including muscular pain. Muscle atrophy is a disease that is characterized with a gradual muscle loss. Muscle atrophy is clearly observed in experimental animals that receive a repeated high-dose of an artificial glucocorticoid, dexamethasone (DEX). This transcriptome analysis aims to investigate the changes in global gene expression profiles in gastrocnemius (GA) and soleus (SO) muscle tissues from mice with DEX-induced muscle atrophy in the presence or absence of JGT co-treatment.

2023-03-21 | GSE227495 | GEO

KLF5 on dexamethasone-mediated atrophy in mouse satellite cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-31 | GSE165072 | GEO

Dexamethasone-induced autophagy mediates muscle atrophy through mitochondrial clearance.

Project description:Glucocorticoids, such as dexamethasone, enhance protein breakdown via ubiquitin-proteasome system. However, the role of autophagy in organelle and protein turnover in the glucocorticoid-dependent atrophy program remains unknown. Here, we show that dexamethasone stimulates an early activation of autophagy in L6 myotubes depending on protein kinase, AMPK, and glucocorticoid receptor activity. Dexamethasone increases expression of several autophagy genes, including ATG5, LC3, BECN1, and SQSTM1 and triggers AMPK-dependent mitochondrial fragmentation associated with increased DNM1L protein levels. This process is required for mitophagy induced by dexamethasone. Inhibition of mitochondrial fragmentation by Mdivi-1 results in disrupted dexamethasone-induced autophagy/mitophagy. Furthermore, Mdivi-1 increases the expression of genes associated with the atrophy program, suggesting that mitophagy may serve as part of the quality control process in dexamethasone-treated L6 myotubes. Collectively, these data suggest a novel role for dexamethasone-induced autophagy/mitophagy in the regulation of the muscle atrophy program.

| S-EPMC4111682 | biostudies-literature

Mechanism of Mitochondrial Dysfunction in Spinal and Bulbar Muscular Atrophy

Project description:This SuperSeries is composed of the SubSeries listed below.

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Quercetin glycosides prevent dexamethasone-induced muscle atrophy in mice.

Project description:Although quercetin has numerous biological benefits, including preventing muscle atrophy due to disuse, no reports have been published to date about the preventive effects and molecular mechanisms underlying drug-induced muscle atrophy. Highly soluble and bioavailable quercetin glycosides (QGs) were used to examine the inhibition of dexamethasone (DEX)-induced muscle atrophy in vivo. Male BALB/cCrSlc mice were treated with or without QGs for 7 days ad libitum, followed by addition of DEX to their drinking water for a further 7 days. The weight of gastrocnemius (GM) adjusted by body weight was significantly decreased on day 7 after DEX treatment. DEX-induced decrease of GM weight was improved by QG co-administration on day 7. The mRNA levels of muscle atrophy-related genes in the gastrocnemius were significantly lowered by QGs on day 1. In particular, the expression of myostatin, a master regulator of muscle mass homeostasis, was suppressed to that of the control level. In murine C2C12 myotubes, quercetin elevated the phosphorylation of Akt, which are downstream of the myostatin pathway, as well as expression of atrogenes. We demonstrated the protective effect of QGs in DEX-induced muscle atrophy, which might depend on the suppression of myostatin signaling.

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Genome-wide analysis of denervation and dexamethasone-responsive gene expression in mouse triceps surae muscle

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-02-12 | E-GEOD-44259 | biostudies-arrayexpress

Samul-tang ameliorates oocyte damage due to cyclophosphamide-induced chronic ovarian dysfunction in mice.

Project description:Samul-tang (SM), a traditional herbal medicine, has been used to treat menstrual irregularities and infertility in women. However, the cellular and molecular mechanisms underlying the effects of SM remain elusive. We investigated the potential protective effect of SM against chronic ovarian dysfunction and used bioinformatics analysis to identify its underlying mechanism in a mouse model of cyclophosphamide (CP)-induced diminished ovarian reserve. Female C57BL/6 mice were intraperitoneally injected with CP three times a week, followed by oral administration of distilled water (CP group) or SM (CP + SM group) for 4 weeks. Four weeks later, the effect of SM was assessed by ovarian tissue histological analysis, steroid hormone measurement, oocyte quality, and mRNA and microRNA microarray analysis in the ovaries. Although SM administration did not prevent CP-induced follicle loss in mice, the quality of oocytes was better in CP + SM mice than in CP mice. Gene expression analysis revealed that the expression of fertilisation- and ovarian follicle development-related genes was altered by CP treatment but normalized after SM administration. Further bioinformatics analysis showed possible interactions between differentially expressed mRNAs and microRNAs. Therefore, we demonstrated the protective effects of SM on ovarian function and oocyte maturation against CP-induced damage via multiple epigenetic mechanisms.

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Reprogramming of Cis-regulatory networks during skeletal muscle atrophy

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-06 | GSE217577 | GEO

MicroRNA 322 Aggravates Dexamethasone-Induced Muscle Atrophy by Targeting IGF1R and INSR.

Project description:Dexamethasone (Dex) has been widely used as a potent anti-inflammatory, antishock, and immunosuppressive agent. However, high dose or long-term use of Dex is accompanied by side effects including skeletal muscle atrophy, whose underlying mechanisms remain incompletely understood. A number of microRNAs (miRNAs) have been shown to play key roles in skeletal muscle atrophy. Previous studies showed significantly increased miR-322 expression in Dex-treated C2C12 myotubes. In our study, the glucocorticoid receptor (GR) was required for Dex to increase miR-322 expression in C2C12 myotubes. miR-322 mimic or miR-322 inhibitor was used for regulating the expression of miR-322. Insulin-like growth factor 1 receptor (IGF1R) and insulin receptor (INSR) were identified as target genes of miR-322 using luciferase reporter assays and played key roles in Dex-induced muscle atrophy. miR-322 overexpression promoted atrophy in Dex-treated C2C12 myotubes and the gastrocnemius muscles of mice. Conversely, miR-322 inhibition showed the opposite effects. These data suggested that miR-322 contributes to Dex-induced muscle atrophy via targeting of IGF1R and INSR. Furthermore, miR-322 might be a potential target to counter Dex-induced muscle atrophy. miR-322 inhibition might also represent a therapeutic approach for Dex-induced muscle atrophy.

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