Exercise-induced methylation of the Serhl2 promoter and implication for lipid metabolism in rat skeletal muscle
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PROVIDER: PRJNA1051971 | ENA |
REPOSITORIES: ENA
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Project description:DNA methylation is an epigenetic mark that influences cell programming and function. Environmental factors such as physical activity alter DNA methylation, with exercise-responsive methylation changes in various tissues including skeletal muscle.
2025-01-22 | GSE250067 | GEO
Project description:We performed transcutaneous electrode stimulation to the tibialis anterior (TA) muscle of rats to mimic resistance exercise and mass spectrometer to measure the changes in protein expression following exercise. Wistar male rats (11-week-old) reared at room temperature (21-25°C) on a 12:12 h light-dark cycle with ad libitum access to food and water. Under isoflurane anaesthesia, isometric contractions of the TA muscle of the rat right leg were induced by skin electrode stimulation using a surface electrode. Protein expression was measured in rat TA muscle before and 12 hours after exercise using a Q Exactive Plus Hybrid Quadrupole-Orbitrap mass spectrometer (Thermo Fisher Scientific).
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Project description:We aimed to investigate the human skeletal muscle (SkM) DNA methylome after exercise in low carbohydrate (CHO) energy balance (with high fat) compared with exercise in low-CHO energy deficit (with low fat) conditions. The objective to identify novel epigenetically regulated genes and pathways associated with ‘train-low sleep-low’ paradigms. The sleep-low conditions included 9 males that cycled to deplete muscle glycogen while reaching a set energy expenditure. Post-exercise, low-CHO meals (protein-matched) completely replaced (using high-fat) or only partially replaced (low-fat) the energy expended. The following morning resting baseline biopsies were taken and the participants then undertook 75 minutes of cycling exercise, with skeletal muscle biopsies collected 30 minutes and 3.5 hours post exercise. Discovery of genome-wide DNA methylation was undertaken using Illumina EPIC arrays and targeted gene expression analysis was conducted by RT-qPCR. At baseline participants under energy balance (high fat) demonstrated a predominantly hypermethylated (60%) profile across the genome compared to energy deficit-low fat conditions. However, post exercise performed in energy balance (with high fat) elicited a more prominent hypomethylation signature 30 minutes post-exercise in gene regulatory regions important for transcription (CpG islands within promoter regions) compared with exercise in energy deficit (with low fat) conditions. Such hypomethylation was enriched within pathways related to: IL6-JAK-STAT signalling, metabolic processes, p53 / cell cycle and oxidative / fatty acid metabolism. Hypomethylation within the promoter regions of genes: HDAC2, MECR, IGF2 and c13orf16 were associated with significant increases in gene expression in the post-exercise period in energy balance compared with energy deficit. Furthermore, histone deacetylase, HDAC11 was oppositely regulated at the gene expression level compared with HDAC2, where HDAC11 was hypomethylated yet increased in energy deficit compared with energy balance conditions. Overall, we identify some novel epigenetically regulated genes associated with train-low sleep-low paradigms.
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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. 18 subjects were divided into 3 groups, performing 12 weeks of Endurance or Strength training or no training. Biopsies for microarray were take before (Pre) and 2½ and 5 hours after the last training session. Isolated RNA from these biopsies were then measured with the Affymetrix Human Gene 1.0 ST arrays.
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Project description:Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training. Keywords: resistance exercise, muscle, aging
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Project description:Colon cancer is the second most cancer type in Europe. Its development is highly influenced by life style factors such as nutrition and physical inactivity. Detailed biological mechanisms are so far unclear. The purpose of this study was to investigate the effects of chronic wheel running on gene expression in rat colon mucosa. Therefore six-week-old male Wistar rats (exercise (EX) group, n=20) completed a stress free voluntary running exercise period of 12 weeks. Sedentary rats served as a control (CO, n=9) group. In the colon mucosa, steady-state mRNA expression levels of approximately 10,000 genes were compared between both groups by micro-array analysis (MWG rat 10k array). 8,846 mRNAs were detected above background level. Chronic exercise led to a decreased expression of 47 genes at a threshold-factor of 2.0. 3 genes were found to be up-regulated in the EX group. The identified genes encode proteins involved in signal transduction (n=11), transport (n=8), immune system (n=7), cytoskeleton (n=6), protein targeting (n=6) and metabolism (n=5). Among the genes regulated by chronic exercise, the betaine-homocysteine methyltransferase 2 (BHMT2) seems to be of particular interest. Physical activity may protect against aberrant methylation by repressing the BHMT2 gene and thus contribute to a decreased risk of developing colon cancer. In summary, our experiment presents the first gene expression pattern in rat colon mucosa following chronic wheel running and therefore represents an important step in understanding the molecular mechanisms responsible for the preventive effect of physical activity on the development of colon cancer. Keywords: voluntary running exercise, animal model
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