Ontology highlight
ABSTRACT:
PROVIDER: PRJNA841859 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21995458.fastq.gz | Fastqsanger.gz | |||
| SRR21995458_1.fastq.gz | Fastqsanger.gz | |||
| SRR21995458_2.fastq.gz | Fastqsanger.gz | |||
| SRR21995459_1.fastq.gz | Fastqsanger.gz | |||
| SRR21995459_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 27 |
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Project description:Standardized muscular biopsies of the dorsal compartment of the gluteus medius muscle were performed in 7 horses suffering from equine polysaccharide storage myopathy (PSSM) and 6 sound Norman Cob horses . Gene expression analysis was performed using an equine oligonucleotide microarray which included 384 equine gene probes of the nuclear genome and all the mitochondrial genes.
2009-04-08 | GSE15572 | GEO
Project description:Standardized muscular biopsies of the dorsal compartment of the gluteus medius muscle were performed in 7 horses suffering from equine polysaccharide storage myopathy (PSSM) and 6 sound Norman Cob horses . Gene expression analysis was performed using an equine oligonucleotide microarray which included 384 equine gene probes of the nuclear genome and all the mitochondrial genes. All the samples of PSSM muscles were hybridized against the reference control muscles. This reference was made by pooling together all the mRNA extracted after in vitro transcription from the 6 control muscles of the sound horses. Briefly, the hybridization protocol was adapted from Le Brigand et al. (2006). An open-access long oligonucleotide microarray resource for analysis of the human and mouse transcriptomes. Nucleic Acids Res. 2006 Jul 19;34(12).
2009-04-08 | E-GEOD-15572 | biostudies-arrayexpress
Project description:Recurrent exertional rhabdomyolysis (RER) develops in 5-10% of Thoroughbred racehorses. High-stress environments, nervous temperament, and diet influence the presentation of RER. RER-susceptibility is associated with alterations in intramuscular Ca2+ regulation with detrimental effects on mitochondria. Our study aims to determine underlying molecular drivers influencing RER-susceptibility by comparing the muscle proteome of control, RER-susceptible, and RER horses treated with dantrolene. Animals used in this study were Thoroughbred mares in race training between episodes of RER.
2021-01-07 | PXD020100 | Pride
Project description:Gene expression profiling in equine polysaccharide storage myopathy
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Project description:During an episode of acute rhabdomyolysis, a microarray study identified differential expression of calcium-regulatory, mitochondrial and metabolic genes in gluteal muscle of Standardbreds. Whether this represents expression related to acute myodegeneration or a specific molecular signature of susceptibility to recurrent exertional rhabdomyolysis (RER) is currently unknown. We compared gluteal muscle histopathology, gene/protein expression and antioxidant concentrations between Standardbreds with a history of, but not currently experiencing rhabdomyolysis, and race-trained controls to derive a molecular susceptibility profile.
2023-03-11 | PXD026121 | Pride
Project description:Equine atypical myopathy (AM) is a severe environmental intoxication linked to the ingestion of protoxins contained in seeds and seedlings of the sycamore maple (Acer pseudoplatanus) in Europe. The toxic metabolites cause a frequently fatal rhabdomyolysis syndrome in grazing horses. Since toxic metabolites can also be present in co-grazing horses, it is still unclear as to why, in a similar environmental context, some horses show signs of AM whereas others remain clinically healthy. Label-free proteomics analyses on the serum of 26 diseased AM, 23 co-grazers and 11 control horses were performed to provide insights into biological processes and pathways. A total of 43 and 44 differentially expressed proteins between “AM vs co-grazing horses” and “AM vs control horses” were found. Disease-linked changes in the proteome of different groups were found to correlate with detected amounts of toxins and principal component analysis was performed to identify the 29 proteins with the greatest impact on the proteomic differences between groups. Among the pathway-specific changes the glycolysis/gluconeogenesis pathway, the coagulation/complement cascade, and the biosynthesis of amino acid were affected. Sycamore maple poisoning results in a combination of inflammation, oxidative stress, and high energy demand, which is trying to be met by enhanced glycolysis.
2024-02-09 | PXD040429 | Pride
Project description:The purpose of this study was to compare the gene expression profile of recurent exercise rhabdomyolysis vs control muscles in French Trotter to determine any metabolic or structural disorder. Transcriptome analysis revealed 191 genes significantly modulated in rhabdomyolysis vs control muscles (p<0.05). Many genes involved in the fatty acid oxidation, the TCA cycle and the mitochondrial respiratory chain were severely down-regulated. The muscle fibers were under hypoxia and oxidative stress conditions which stimulated glycolysis. The muscle fiber calcium homeostasis was greatly affected towards an increase of cytoplasmic calcium and a depletion of the sarcoplasmic reticulum calcium. Gene expression analysis revealed an alteration of the aerobic ATP synthesis with a severe mitochondrial dysfunction which could explain the disruption of the cytoplasmic calcium regulation and a muscular relaxation disorder. Total RNA was extracted from the gluteal medius and longissimus lumborum muscles after biopsies in 15 French Trotter horses including 10 controls and 5 RER horses affected by rhabdomyolysis with high plasmatic muscular enzyme activities. Gene expression analysis was performed on the muscle biopsies using a 25K oligonucleotide microarray.
2010-12-15 | E-GEOD-26047 | biostudies-arrayexpress
Project description:Pompe disease is a Lysosomal glycogen storage disorder due to the deficiency of acid alpha glucosidase. The enzyme degrades glycogen to glucose and its deficiency results in progressive enlargement of glycogen-filled lysosomes in multiple tissues with skeletal and cardiac muscle most severely affected clinically. Clinical spectrum ranges from most severe infantile cardiomegally and skeletal muscle myopathy to milder late onset forms with only skeletal muscle pathology. The currently available enzyme replacement therapy has only limited effect in skeletal muscle. Here we use RNA sequencing of therapy-resistant skeletal muscle (white part of gastrocnemius muscle) to identify the differencies between the diseased and healthy muscle. Total RNA was obtained from gastrocnemius muscle (white part) of acid alpha glucosidase knock-out and wild-type mice.
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Project description:aCGH performed to identify copy number variants in Quarter Horses and perform casec-control GWAS
2014-05-10 | GSE57510 | GEO
Project description:As a consequence of impaired glucose or fatty acid metabolism, bioenergetic stress in skeletal muscles may trigger myopathy and rhabdomyolysis. Genetic mutations causing loss of function of the LPIN1 gene frequently lead to severe rhabdomyolysis bouts in children, though the metabolic alterations and possible therapeutic interventions remain elusive. Here, we show that lipin1 deficiency in mouse skeletal muscles is sufficient to trigger myopathy. Strikingly, muscle fibers display strong accumulation of both neutral and phospholipids. The metabolic lipid imbalance can be traced to an altered fatty acid synthesis and fatty acid oxidation, accompanied by a defect in acyl chain elongation and desaturation. As an underlying cause, we reveal a severe sarcoplasmic reticulum (SR) stress, leading to the activation of the lipogenic SREBP1c/SREBP2 factors, the accumulation of the Fgf21 cytokine, and alterations of SR-mitochondria morphology. Importantly, pharmacological treatments with the chaperone TUDCA and the fatty acid oxidation activator bezafibrate improve muscle histology and strength of lipin1 mutants. Our data reveal that SR stress and alterations in SR-mitochondria contacts are contributing factors and potential intervention targets of the myopathy associated with lipin1 deficiency.
2019-01-07 | MTBLS750 | MetaboLights