MicroRNA expression during skeletal muscle differentiation and exercse in skeletal muscle.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE29286 | GEO | 2011/05/14
SECONDARY ACCESSION(S): PRJNA141615
REPOSITORIES: GEO
Similar Datasets
Project description:To investigate microRNAs related to mitochondria biogenesis in skeletal muscle, microRNA expressions during skeletal muscle differentiation and exercise were analyzed in vivo and in vitro. Murine skeletal muscle cell (C2C12) were assigned to undifferentiated, differentiated, and passively stretched (exercise mimicked). C57BL/6S mice were assigned to resting, acute exercise (1day), and chronic exercise (7days). Low molecular weight RNA (< 200 nucleotides) was isolated from C2C12 cell or tibialis anterior muscle of mice and hybridized to Ncode microRNA microarrays. The experiment was performed using a loop design for the data analysis.
2011-05-14 | E-GEOD-29286 | biostudies-arrayexpress
Project description:To identify changes in skeletal muscle microRNA expression after exercise and associate the identified microRNAs with mRNA and protein expression to disease-specific pathways in polymyositis and dermatomyositis
2017-10-31 | GSE95772 | GEO
Project description:To identify changes in skeletal muscle microRNA expression after exercise and associate the identified microRNAs with mRNA and protein expression to disease-specific pathways in polymyositis and dermatomyositis
2017-10-31 | GSE95735 | GEO
Project description:Ribosomes are the macromolecular engines of protein synthesis. Factors mediating ribosome biogenesis in skeletal muscle that facilitate adaptation to exercise are multi-factorial, but may be related to ribosomal DNA (rDNA) dosage and/or epigenetic modifications to rDNA. To investigate these possibilities, we conducted reduced representation bisulfite sequencing (RRBS) on skeletal muscle biopsies from human subjects before and after exercise and to detect differences in methylation patterns during exercise adaptation.
2021-07-13 | GSE162392 | GEO
Project description:This experiment was conducted to identify target microRNAs of the peroxisome proliferator-activated receptor (PPAR) in skeletal muscle of transgenic mice that overexpressed PPARalpha or PPARbeta. We have recently demonstrated that skeletal muscle-specific PPARb transgenic (MCK-PPARb) mice exhibit increased exercise endurance, whereas MCK-PPARa mice have reduced exercise performance. Accordingly, we sought to determine whether PPARb and PPARa drive distinct programs involved in muscle fiber type determination. Myosin heavy chain (MHC) immunohistochemical staining of soleus muscle revealed a marked increase in type 1 fibers in the MCK-PPARb muscle compared to non-transgenic (NTG) littermates but a profound reduction in MCK-PPARa muscle. miRNA profiling revealed that levels of miR-208b and miR-499 were increased in MCK-PPARb muscle but reduced in MCK-PPARa muscle. miR-208b and miR-499, which are embedded in the Myh7 and Myh7b genes, respectively, have been shown previously to regulate slow-twitch muscle genes. Lastly, combined inhibition of miR-208b and miR-499 abolished the enhancing effects of PPARb on MHC1 expression in skeletal myotubes, while forced expression of miR-499 in MCK-PPARa muscle completely reversed the type 1 fiber program and exercise capacity. Taken together, these findings demonstrate that miR-208b and miR-499 are necessary to mediate the effects of PPARb and PPARa on muscle fiber type determination. Comparison of microRNA expression from soleus muscles isolated from wild-type (non-transgenic (NTG)) and PPARalpha-overexpressing (MCK-PPARa) mice, and comparison of microRNA expression from soleus muscles isolated from wild-type (NTG) and PPARbeta-overexpressing (MCK-PPARb) mice. Three replicates of each are analyzed.
2013-05-09 | E-GEOD-36498 | biostudies-arrayexpress
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:Exercise is an important strategy in the prevention and treatment of metabolic diseases, like diabetes and obesity. Alterations in the skeletal muscle proteome, including post-translational modifications, especially acetylation, regulate its metabolic adaptations to exercise. Here, we examined the effect of 6-week aerobic exercise and Scriptaid, a HDAC4/5 inhibitor, on the proteome and acetylome of skeletal muscle in mice. We find Scriptaid and exercise both induce acetylation modification changes of some proteins involved in metabolism, suggest that exercise improves metabolic health by regulating protein acetylation level.
2022-04-06 | PXD032660 | iProX
Project description:Exercise Mitigates Skeletal Muscle Epigenetic Aging
| PRJNA732356 | ENA
Project description:The few investigations on exercise-induced global gene expression responses in human skeletal muscle haves typically focused at one specific mode of exercise and few such studies have implemented control measures. However, interpretation on distinct phenotype regulation necessitate comparison between essentially different modes of exercise and the ability to identify true exercise effects, necessitate implementation of independent non-exercise control subjects. Furthermore, muscle transkriptometranscriptome data made available through previous exercise studies can be difficult to extract and interpret by individuals that are inexperienced with bioinformatic procedures. In a comparative study, we; (1) investigated the human skeletal muscle transcriptome response to differentiated exercise and non-exercise control intervention, and; (2) aimed to develop a straightforward search tool to allow for easy extraction and interpretation of our data. We provide a simple spreadsheet containing transcriptome data allowing other investigators to see how mRNA of their interest behave in skeletal muscle following exercise, both endurance, strength and non-exercise. Our approach, allow investigators easy access to information on genuine transcriptome effects of differentiated exercise, to better aid hyporthesis-driven question in this particular field of research.
2014-11-19 | GSE59088 | GEO
Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.
2019-08-01 | GSE130839 | GEO