E-GEOD-31839
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-31839 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-31839-analysis-methods.tsv | Tabular | |||
| E-GEOD-31839-analytics.tsv | Tabular | |||
| E-GEOD-31839-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-31839-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-31839-analytics.tsv.unrounded | Tabular |
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Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE31839: Effect of wheel running exercise and myostatin depletion on gene expression in triceps brachii muscles of mice GSE31843: Effect of wheel running exercise on gene expression in skeletal muscles of mice Refer to individual Series
2011-09-02 | E-GEOD-31844 | biostudies-arrayexpress
Project description:The purpose of this study was to determine whether postdevelopmental myostatin depletion influenced the changes in skeletal muscle gene expression profiles induced by a long-term increase in physical activity. Myostatin levels in muscles of adult male mice with floxed myostatin genes were reduced ~85% by activating Cre recombinase. Control mice with normal myostatin genes had the same Cre-activating treatment. Some of the mice were housed in ordinary cages throughout the study, limiting their physical activity. Other mice were given free access to running wheels for the final 12 weeks of the study. At the end of the study, comprehensive gene expression profiles of triceps brachii muscles were determined by RNA sequencing (RNA-Seq), with muscles from mice selected for similarity of running behavior throughout the period of wheel access. Wheel running increased expression of hundreds of mRNAs encoding proteins involved in oxidative energy metabolism, and this response was not affected by myostatin deficiency. The running-induced increase in the ratio of Myh1 mRNA (which encodes myosin heavy chain type 2x) to Myh4 mRNA (which encodes myosin heavy chain type 2b) also was not affected by myostatin depletion. At every threshold of P (computed by analysis of variance), the number of transcripts with interactions between activity level and myostatin level was fewer than the number expected by chance. These data suggest that myostatin is not required for transcriptional adaptations to moderate-intensity exercise. 12 samples, 6 from sedentary mice and 6 from active (wheel running) mice. 3 control and 3 myostatin-deficient mice within each activity level.
2011-09-02 | E-GEOD-31839 | biostudies-arrayexpress
Project description:The purpose of this study was to determine whether postdevelopmental myostatin depletion influenced the changes in skeletal muscle gene expression profiles induced by a long-term increase in physical activity. Myostatin levels in muscles of adult male mice with floxed myostatin genes were reduced ~85% by activating Cre recombinase. Control mice with normal myostatin genes had the same Cre-activating treatment. Some of the mice were housed in ordinary cages throughout the study, limiting their physical activity. Other mice were given free access to running wheels for the final 12 weeks of the study. At the end of the study, comprehensive gene expression profiles of triceps brachii muscles were determined by RNA sequencing (RNA-Seq), with muscles from mice selected for similarity of running behavior throughout the period of wheel access. Wheel running increased expression of hundreds of mRNAs encoding proteins involved in oxidative energy metabolism, and this response was not affected by myostatin deficiency. The running-induced increase in the ratio of Myh1 mRNA (which encodes myosin heavy chain type 2x) to Myh4 mRNA (which encodes myosin heavy chain type 2b) also was not affected by myostatin depletion. At every threshold of P (computed by analysis of variance), the number of transcripts with interactions between activity level and myostatin level was fewer than the number expected by chance. These data suggest that myostatin is not required for transcriptional adaptations to moderate-intensity exercise.
2011-09-03 | GSE31839 | GEO
Project description:To gain insight into the mechanisms by which exercise affects the muscle stem cell compartment, we subjected young and old mice to aerobic exercise and performed single cell transcriptome analysis of mononucleated cells from hindlimb muscles of these animals.
2023-04-19 | GSE196361 | GEO
Project description:Effect of wheel running exercise and myostatin depletion on gene expression in triceps brachii muscles of mice
| PRJNA155263 | ENA
Project description:Exercise training increases endurance by inducing global gene expression changes in skeletal muscles. The extent to which the genetic effects of exercise can be mimicked by synthetic drugs is unknown. We measured global skeletal muscle expression in sedentary and exercised mice treated with vehicle or PPARdelta ligand GW1516. PPARdelta is a transcriptional regulator of muscle oxidative metabolism and fatigue resistance. Experiment Overall Design: Sedentary and exercise trained C57Bl/6J mice were treated with vehicle or GW1516 for 4 weeks, followed by collection of quadriceps for gene expression analysis.
2008-10-21 | E-GEOD-11803 | biostudies-arrayexpress
Project description:Appropriate amount of exercise is the best way to prevent various diseases and have a healthy life. Skeletal muscles communicate with other organs through myokines, which are secreted by muscle itself during exercise and elicit various effects in the body. However, despite the years of efforts to understand molecular mechanisms of crosstalk between muscle and other organs that mediate the beneficial effects of exercise are not completely understood. To identify novel myokines, we used an in vitro exercise model in C2C12 cells using the electrical pulse stimulation (EPS) that can mimic muscle contraction. We generated RNA-seq data of seven in vitro samples to costruct a prediction model based on differentially expressed genes, showing significantly mimicking in vivo exercise.
2022-12-14 | GSE176563 | GEO
Project description:Understanding the relationship between physical exercise, reactive oxygen species and skeletal muscle modification is important in order to better identify the benefits or the damages that appropriate or inappropriate exercise can induce. Heart and skeletal muscles have a high density of mitochondria with robust energetic demands and mitochondria plasticity has an important role in both cardiovascular system and skeletal muscle responses. The aim of this study was to investigate the influence of regular physical activity on oxidation profiles of mitochondrial proteins from heart and tibialis anterior muscles. To this end, we used mouse as animal model. Mice were divided in two groups: untrained and regularly trained. The carbonylated protein pattern was studied by two-dimensional gel electrophoresis followed by Western Blot with anti-dinitrophenyl hydrazone antibodies. Mass spectrometry analysis allowed the identifications of several different protein oxidation sites including methionine, cysteine, proline and leucine residues. A large number of oxidized protein were found in both untrained and trained animals. Moreover, mitochondria from skeletal muscles and heart showed almost the same carbonylation pattern. Interestingly, exercise training seems to increase carbonylation level mostly of mitochondrial protein from skeletal muscle.
2022-02-24 | PXD003982 | Pride
Project description:We show that the orphan nuclear receptor ERRg is expressed at high levels in type I muscle and when transgenically expressed in anaerobic type II muscles (ERRGO mice) or cultured cells, powerfully regulates VEGF expression, angiogenesis and vascular supply in absence of exercise. ERRGO mice show increased expression of genes promoting fat metabolism, mitochondrial respiration and type I fiber specification. In parallel, the type II muscle in ERRGO mice display an activated angiogenic program marked by myofibrillar induction and secretion of pro-angiogenic factors, frank neo-vascularization and a 100% increase in running endurance. Surprisingly, the induction of VEGF and type I muscle properties by ERRg does not involve the transcriptional co-activator PGC1a. Instead, ERRg genetically activates the energy sensor AMPK which is typically inactive in absence of exercise. Therefore, ERRg and AMPK, known regulators of mitochondrial function and metabolism, together control a novel angiogenic pathway that anatomically synchronizes vascular arborization to oxidative metabolism revealing an exercise-independent mechanism for matching supply and demand. Keywords: ERRgamma overexpression compared to wild-type Comparison of gene expression from quadriceps muscles isolated from wild type and alpha-skeletal actin-ERRgamma-transgenic mice.
2011-09-18 | E-GEOD-22086 | biostudies-arrayexpress
Project description:Exercise training increases endurance by inducing global gene expression changes in skeletal muscles. The extent to which the genetic effects of exercise can be mimicked by synthetic drugs is unknown. We measured global skeletal muscle expression in sedentary and exercised mice treated with vehicle or PPARdelta ligand GW1516. PPARdelta is a transcriptional regulator of muscle oxidative metabolism and fatigue resistance. Keywords: Pharmacology study
2008-06-18 | GSE11803 | GEO