Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1099435 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28699512_1.fastq.gz | Fastqsanger.gz | |||
| SRR28699512_2.fastq.gz | Fastqsanger.gz | |||
| SRR28699513_1.fastq.gz | Fastqsanger.gz | |||
| SRR28699513_2.fastq.gz | Fastqsanger.gz | |||
| SRR28699514_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
Similar Datasets
Project description:Ischemic preconditioning is the phenomenon whereby brief periods of sublethal ischemia protect against a subsequent, more prolonged, ischemic insult. In remote ischemic preconditioning (RIPC), ischemia to one organ protects other organs at a distance. We developed mouse models to ask if inhibition of EglN1, which senses oxygen and regulates the HIF transcription factor, could suffice to mediate local and remote ischemic preconditioning. We used microarrays to detail the global expression changes induced when the oxygen sensor EglN1 is genetically deleted from skeletal muscle cells. We also used microarrays to assess the transcriptome alterations that occur in mouse hearts with pharmacologic inhibition of EglN1, using the EglN inhibitor FG-4497. We generated mice with a tamoxifen-inducible model of EglN1 loss using a floxxed EglN1 locus with skeletal muscle-specific CRE recombinase. WT mice and mice with the floxxed EglN1 locus were exposed to tamoxifen. Mouse skeletal muscle was isolated for RNA extraction and hybridization on Affymetrix microarrays. In a related experiment, mice were treated with the EglN inhibitor FG-4497, and RNA from their heart tissue was analyzed by microarray for transcriptome alterations compared to control hearts.
2016-02-11 | E-GEOD-77789 | biostudies-arrayexpress
Project description:Purpose: dissolved oxygen (DO) level is an important factor that could significantly influence microorganisms’ growth, maintenance, metabolism and product yield. The goals of this study are to do comparative analysis on Corynebacterium glutamicum transcriptome in response to the change of dissolved oxygen in bioreactor, find the critical pathways and genes.
2016-02-03 | GSE77502 | GEO
Project description:Purpose:dissolved oxygen (DO) level is an important factor that could significantly influence microorganisms’ growth, maintenance, metabolism and product yield.The goals of this study are to comparative analysis on Corynebacterium glutamicum transcriptome in response to expression of eGFP under the change of dissolved oxygen in bioreactor,find the critical pathways and genes.
2016-09-20 | GSE87077 | GEO
Project description:Duchenne muscular dystrophy (DMD) is caused by genetic deficiency of dystrophin and characterized by massive structural and functional changes of skeletal muscle tissue, leading to terminal muscle failure. In this project, proteomics data from skeletal muscle of a genetically engineered DMD pig model treated by somatic gene editing are shown.
2020-02-05 | PXD014893 | Pride
Project description:Muscular dystrophy is a group of diseases that cause progressive weakness and degeneration of the skeletal muscles that control movement. Lacking polymerase I transcription release factor (PTRF, also known as Cavin1), an essential caveolae component, causes a secondary deficiency of caveolins resulting in muscular dystrophy. Because skeletal muscle is a heterogeneous tissue composed of different metabolic muscle fiber (myofibers) and mononuclear cells, the transcriptome responses of these myofibers and mononuclear cell to muscular dystrophy caused by PTRF deletion has not been explored. Here, we create muscular dystrophy mice caused by the deletion of PTRF gene and apply single-nucleus RNA sequencing (snRNA-seq) to unveil transcriptional changes in the skeletal muscle of mice with muscular dystrophy at single-nucleus resolution.
2023-05-31 | GSE217390 | GEO
Project description:Duchenne muscular dystrophy (DMD) is caused by genetic deficiency of dystrophin and characterized by massive structural and functional changes of skeletal muscle tissue, leading to terminal muscle failure. In this project, proteomics data from skeletal muscle of a genetically engineered DMD pig model were investigated in order to confirm muscular fibrosis and MSOT signals.
2020-01-09 | PXD016003 | Pride
Project description:Context: Exercise training is a plausible model for identification of molecular mechanisms that cause metabolic-related changes in human skeletal muscle. Objective: The goal was to explore the molecular basis of the adaptation of skeletal muscle to exercise training. Design and Intervention: Obese male subjects were subjected to an individualized supervised training program targeted in order to optimize lipid oxidation during 8 weeks. Main Outcome Measures: Primary outcome measures were gene expression profiling of skeletal muscle. Body composition, oral glucose tolerance test, Resting metabolic rate, respiratory quotient, maximal oxygen uptake and metabolic biochemistry were also assessed. Overall Design The obese (BMI 30-36) male volunteers (age 32-42) were asked to refrain from vigorous physical activity 48h before presenting to the clinical investigation centre, and ate a weight-maintaining diet consisting of 35% fat, 16% protein, and 49% carbohydrates two days before the experiment. Muscle biopsies of Vastus Lateralis weighing 60–100 mg were obtained using the Bergstrom technique, cleaned and snap-frozen in liquid nitrogen. Resting metabolic rate, respiratory quotient and maximal oxygen uptake were assessed. The subjects were investigated at baseline and after 8 weeks of supervised aerobic exercise training program consisting of daily sessions of 45-60 min of endurance exercise, 5 days a week, at least 48-72h after the last acute exercise bout. Skeletal muscle biopsies were obtained at the beginning and at the end of the protocol. Transcriptome analysis compared 8 subjects before vs. after training using arrays using a common reference design (Cy5 dye was incorporated into all muscle RNA samples, while a reference RNA pool made of the mix of commercial human liver, adipose tissue and skeletal muscle RNA was labelled with Cy3 dye (Applied Biosystems/Ambion, Foster City, USA)( and whole genome 4x44k oligonucleotide arrays (Agilent Technologies).
2012-12-10 | E-GEOD-40551 | biostudies-arrayexpress
Project description:Skeletal muscle is the largest tissue in the body and mainly relies on mitochondrial oxidative metabolism for sustainable ATP production. Reduced oxygen availability, also known as hypoxia, can be caused by high altitude or pathology and impacts mitochondria. Whereas long-term hypoxia results in increased reliance on glycolysis, reduced fatty acid oxidation and a decreased skeletal muscle mass, the in vivo mechanisms of adaptation of skeletal muscle to acute hypoxia remain elusive. Therefore, we aimed to provide an integrated description of the response of the M. gastrocnemius to acute hypoxia. Fasted male C57BL/6JOlaHsd mice were exposed to 12% oxygen representing normobaric hypoxia versus 21% oxygen (normoxia) for six hours (n=12 mice per group). Whole-body energy metabolism and the transcriptome response of the M. gastrocnemius mice was analyzed and confirmed by acylcarnitine determination and RT-qPCR. On whole-body level, six hours of hypoxia reduced energy expenditure, increased blood glucose and tended to further decrease the respiratory exchange ratio (RER). Whole genome transcriptome analysis revealed upregulation of the FOXO signalling pathway including an increased expression of Trib3, which was positively correlated with blood glucose. Apart from upregulation of Cpt1a, which negatively correlated with the RER, and SLC25a25 (Cact), fatty acid β-oxidation was not regulated. Together with significantly increased muscle C14 and C16-acylcarnitines this supports no increased fatty acid catabolism in muscle. In addition, the hypoxia-induced FOXO activation could also be connected to altered gene profiles related to fiber type switching, extracellular matrix remodelling, muscle differentiation and the denervation of neuromuscular junctions (NMJ). Conclusively, our results suggest that an acute, six hours exposure of mice to hypoxia impacts M. gastrocnemius via FOXO1, initiating alterations in skeletal muscle that may ultimately contribute to tissue remodelling. This supports an early role of hypoxia in tissue alterations in hypoxia-associated conditions such as aging and obesity. The observed impact of hypoxia on denervated NMJ is novel and warrants further investigation.
2023-10-23 | GSE228719 | GEO