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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from 2-amino acetophenone (2-AA) treated mouse Skeletal muscle

ABSTRACT: Metabolic responses begin promptly upon the initiation of infection, and progress as a series of coordinated events. Mitochondria may play a key role in the development of insulin resistance. Reduced energy production and mitochondrial dysfunctional may further favor infection, and be an important step in the establishment of chronic and persistent infections. We have used mouse skeletal muscle transcriptome data which have led to the hypothesis that 2-AA causes harm to the host by triggering mitochondrial dysfunction in skeletal muscle. The gastrocnemius muscles were isolated from control and 4days 2-AA treated mouse for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Laurence Rahme

PROVIDER: E-GEOD-43779 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from 2-amino acetophenone (2-AA) treated mouse Skeletal muscle

Project description:Metabolic responses begin promptly upon the initiation of infection, and progress as a series of coordinated events. Mitochondria may play a key role in the development of insulin resistance. Reduced energy production and mitochondrial dysfunctional may further favor infection, and be an important step in the establishment of chronic and persistent infections. We have used mouse skeletal muscle transcriptome data which have led to the hypothesis that 2-AA causes harm to the host by triggering mitochondrial dysfunction in skeletal muscle.

2013-01-28 | GSE43779 | GEO

Effects of siRNA depletion on gene expression during C2C12 skeletal muscle differentiation initiation

Project description:In humans, skeletal muscles comprise nearly 40% of total body mass, which is maintained throughout adulthood by a balance of muscle protein synthesis and breakdown. Cellular amino acid (AA) levels are critical for these processes, and mammalian cells contain transporter proteins that import AAs to maintain homeostasis. Until recently, the control of transporter regulation has largely been studied at the transcriptional and post-translational levels; however, our recent work demonstrates that the RNA-binding protein YBX3 is critical to intracellular sustain AA in human cells. Here we report that YBX3 post-transcriptionally controls the levels of specific AA transporter messenger (m)RNAs in skeletal muscle cells, which impacts the intracellular levels transported by these proteins. Further, we find that reduction of YBX3 protein reduces proliferation during skeletal muscle differentiation, and that YBX3 expression increases substantially during skeletal muscle differentiation, which is independent to changes in itsmRNA levels. Taken together, our findings suggest that YBX3 regulates AA transport in skeletal muscle cells and that its expression is critical to maintain skeletal muscle cell proliferation during differentiation.

2023-12-20 | GSE240445 | GEO

A systems study reveals concurrent activation of AMPK and mTOR by amino acids

Project description:Amino acids (aa) are not only building blocks for proteins, but also signalling molecules, with the mammalian target of rapamycin complex 1 (mTORC1) acting as a key mediator. However, little is known about whether aa, independently of mTORC1, activate other kinases of the mTOR signalling network. To delineate aa-stimulated mTOR network dynamics, we here combine a computational–experimental approach with text mining-enhanced quantitative proteomics. We report that AMP-activated protein kinase (AMPK), phosphatidylinositide 3-kinase (PI3K) and mTOR complex 2 (mTORC2) are acutely activated by aa-readdition in an mTORC1-independent manner. AMPK activation by aa is mediated by Ca2+/calmodulin-dependent protein kinase kinase β (CaMKKβ). In response, AMPK impinges on the autophagy regulators Unc-51-like kinase-1 (ULK1) and c-Jun. AMPK is widely recognized as an mTORC1 antagonist that is activated by starvation. We find that aa acutely activate AMPK concurrently with mTOR. We show that AMPK under aa sufficiency acts to sustain autophagy. This may be required to maintain protein homoeostasis and deliver metabolite intermediates for biosynthetic processes.

2016-12-12 | PXD003073 | Pride

Expression data from murine myogenic cells

Project description:Skeletal muscle has great regenerative capacity, which is dependent on muscle stem cells, also known as satellite cells. We established the purification system of myogenic cells. We used microarrays to identify specific genes during the muscle regenerative process. Myogenic cells were purified at regenerative stages for RNA extraction and hybridization on Affymetrix microarrays. CTX-2d and CTX-5d are the samples derived from injured muscles 2 days and 5 days after cardiotoxin-injection, respectively.

2014-07-01 | E-GEOD-56903 | biostudies-arrayexpress

Muscle from patients with mitochondrial myopathies and congenital muscular dystrophies versus normal human muscle

Project description:Global gene expression analysis was performed comparing human skeletal muscle samples from patients with various forms of muscular dystrophy and mitochondrial myopathies in order to identify specific gene expression changes associated with collagen VI deficiency (leading to UllrichM-BM-4s Congenital Muscular Dystrophy) and depletion of mitochondrial DNA relative to other mitochondrial myopathies We analysed the gene expression profile of skeletal muscle from children suffering from mitochondrial myopathies and various forms of muscular dystrophy relative to skeletal muscle from healthy children using commercially available arrays that represents the complete human genome (Agilent Human SurePrintGE, 8x60K )

2015-01-20 | E-GEOD-43698 | biostudies-arrayexpress

Muscle fiber transdifferentiation in an experimental model of respiratory chain myopathy

Project description:Skeletal muscle fiber composition and muscle energetics are not static and change in muscle disease. This study was performed to determine if a mitochondrial myopathy is associated with adjustments in skelatal fiber type composition. These effects of drug induced mitochondrial dysfunction on skeletal muscle fiber type composition were analyzed in an animal model.

2012-10-18 | E-MEXP-3642 | biostudies-arrayexpress

Mitofusin 2 expression in muscle decreases during aging and generates a gene signature characteristic of aged muscle

Project description:Mitochondrial fusion and fission proteins regulate mitochondrial quality control and mitochondrial metabolism. In turn, mitochondrial dysfunction is associated with aging, although its causes are still under debate. Here, we show that aging is characterized by a progressive reduction of Mitofusin 2 (Mfn2) in mouse skeletal muscle and that skeletal muscle Mfn2 ablation in mice generates a gene signature linked to aging. Furthermore, muscle Mfn2-deficient mice show unhealthy aging characterized by altered metabolic homeostasis and sarcopenia. Mfn2 deficiency impairs mitochondrial quality control, which contributes to an exacerbated age-related mitochondrial dysfunction. Surprisingly, aging-induced Mfn2 deficiency triggers a ROS-dependent retrograde signaling pathway through induction of HIF1 transcription factor and BNIP3. This pathway ameliorates mitochondrial autophagy and minimizes mitochondrial damage. Our findings reveal that repression of Mfn2 in skeletal muscle during aging is determinant for the loss of mitochondrial quality, contributing to age-associated metabolic alterations and loss of muscle fitness. Quadriceps muscle from four mice per genotype were used (Control young (6 month-old), Mfn2KO young (6-month-old), control old (22-month-old) and Mfn2KO old (22-month-old)

2016-08-08 | E-GEOD-71501 | biostudies-arrayexpress

Skeletal muscle PGC-1a mediates mitochondrial, but not metabolic, changes during calorie restriction.

Project description:Calorie restriction (CR) is a dietary intervention that extends lifespan and healthspan in a variety of organisms. CR improves mitochondrial energy production, fuel oxidation and reactive oxygen species scavenging in skeletal muscle and other tissues, and these processes are thought to be critical to the benefits of CR. PGC-1a is a transcriptional coactivator that regulates mitochondrial function and is induced by CR. Consequently, many of the mitochondrial and metabolic benefits of CR are attributed to increased PGC-1a activity. To test this model for the first time, we examined the metabolic and mitochondrial response to CR in mice lacking skeletal muscle PGC-1a (MKO). Surprisingly, MKO mice demonstrated a normal improvement in glucose homeostasis in response to CR, indicating that skeletal muscle PGC-1a is dispensable for the whole-body benefits of CR. In contrast, gene expression profiling and electron microscopy demonstrated that PGC-1a is required for the full CR-induced increases in mitochondrial gene expression and mitochondrial density in skeletal muscle. These results demonstrate that PGC-1a is a major regulator of the mitochondrial response to CR in skeletal muscle, but surprisingly show that neither PGC-1a nor mitochondrial biogenesis in skeletal muscle are required for the metabolic benefits of CR. Control (FLOX) and PGC-1a skeletal muscle specific knock out (MKO) mice were placed on a control diet [C] or a calorie restriction diet [CR] for 12 weeks. RNA was isolated from TA/EDL muscles for microarray analysis. The following numbers of mice were analyzed from each group: C FLOX: n = 6; C MKO: n = 7; CR FLOX: n = 6; CR MKO: n = 7. Mice were mixed C57/BL6 and 129 background.

2012-02-04 | E-GEOD-34773 | biostudies-arrayexpress

Expression data of Col:LUC Arabidopsis treated with antimycin A (AA) in the presence or absence of a synthetic auxin analogue

Project description:Mitochondrial stress stimuli such as AA caused a transient suppression of auxin signaling and conversely, auxin treatment represses a part of the response to AA treatment. Expression data of Col:LUC Arabidopsis treated with antimycin A (AA) in the presence or absence of a synthetic auxin analogue Total RNA extraction was carried out on 80 mg of Col:LUC Arabidopsis seedlings grown on B5 media for 10 days and transferred to fresh plates, containing either B5 media or B5 media supplemented with 4.5 µM NAA for an additional 3 days. Seedlings were treated with 50 µM AA for 3 hours.

2014-06-01 | E-GEOD-57140 | biostudies-arrayexpress

Drp1 regulates mitochondrial health and controls skeletal muscle mass through the Erk1/2-Nur77 pathway

Project description:The maintenance of skeletal muscle mass is critically dependent upon mitochondrial quality control, including balanced mitochondrial dynamics and mitophagy. Dynamin-related protein 1 (Drp1), a key mediator of mitochondrial fission, plays an important role in these processes. However, the precise mechanisms by which Drp1 regulates mitochondrial integrity and muscle mass remain inadequately understood. Here, we show that acute Drp1 deletion from skeletal muscle impairs mitochondrial activity, increases Parkin-mediated mitophagy, progressively reduces mitochondrial DNA (mtDNA) content, and ultimately causes severe muscle atrophy. Interestingly, dual deletion of Drp1 and Parkin from skeletal muscle restored mtDNA content, but did not prevent muscle loss. Mechanistically, Drp1 deletion disrupted mitochondrial respiratory chain activity, which suppressed extracellular signal-regulated kinase 1/2 (Erk1/2) signaling and downregulated the nuclear receptor subfamily 4 group member 1 (Nur77), a regulator of muscle quality. Finally, clenbuterol, a β2-adrenergic receptor agonist, activated Erk1/2 signaling, restored Nur77 expression, and rescued muscle atrophy. Collectively, our findings identify a Drp1-Erk1/2-Nur77 signaling axis that connects mitochondrial integrity to the preservation of skeletal muscle mass and represents a potential therapeutic avenue for muscle degeneration in mitochondrial and metabolic disorders.

2025-12-08 | GSE295479 | GEO

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