E-GEOD-52550
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA229363
PROVIDER: E-GEOD-52550 | ExpressionAtlas | 2015-07-29
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-52550-analysis-methods.tsv | Tabular | |||
| E-GEOD-52550-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-52550-configuration.xml | Xml | |||
| E-GEOD-52550-percentile-ranks.tsv | Tabular | |||
| E-GEOD-52550.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 68 |
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Project description:Progressive loss of PGC-1alpha expression in aging muscle potentiates glucose intolerance and systemic inflammation
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Project description:Aging of skeletal muscle tissue is characterized by loss of metabolic and contractile competence. It is thought that this phenomenon is driven via extrinsic and intrinsic factors. In order to identify age-dependent changes intrinsic to the muscle cell, microarray transcriptional profiles and measurements of glucose metabolism were performed in primary cultured human myotubes at different time points over seven weeks. Aging in culture tended to reduce myotube glucose metabolism, oxidative and storage capacities, despite elevation of glucose transport. The mitochondrial membrane potential slightly increased, whereas peroxidation of cell membrane lipids declined and membrane integrity was preserved. Transcriptional analysis revealed a fall in genes involved in glucose metabolism and oxidative phosphorylation, while stress defense genes were elevated. Expression of numerous genes coding for muscle contractile proteins and calcium-regulating proteins, was gradually decreased during aging of cultured myotubes. Transcripts of genes involved in cell growth, matrix and motility markedly rose while those involved in cell adhesion dropped. In conclusion, aging myotubes in culture exhibit a loss of glucose metabolic capacity. They are characterized by a shift from a contractile to a growth-survival, matrix-remodeling phenotype. This pattern of changes, linked to intrinsic factors, displays significant similarities with aging of muscle from primates and human subjects.
2007-07-19 | E-GEOD-1144 | biostudies-arrayexpress
Project description:Aging of skeletal muscle tissue is characterized by loss of metabolic and contractile competence. It is thought that this phenomenon is driven via extrinsic and intrinsic factors. In order to identify age-dependent changes intrinsic to the muscle cell, microarray transcriptional profiles and measurements of glucose metabolism were performed in primary cultured human myotubes at different time points over seven weeks. Aging in culture tended to reduce myotube glucose metabolism, oxidative and storage capacities, despite elevation of glucose transport. The mitochondrial membrane potential slightly increased, whereas peroxidation of cell membrane lipids declined and membrane integrity was preserved. Transcriptional analysis revealed a fall in genes involved in glucose metabolism and oxidative phosphorylation, while stress defense genes were elevated. Expression of numerous genes coding for muscle contractile proteins and calcium-regulating proteins, was gradually decreased during aging of cultured myotubes. Transcripts of genes involved in cell growth, matrix and motility markedly rose while those involved in cell adhesion dropped. In conclusion, aging myotubes in culture exhibit a loss of glucose metabolic capacity. They are characterized by a shift from a contractile to a growth-survival, matrix-remodeling phenotype. This pattern of changes, linked to intrinsic factors, displays significant similarities with aging of muscle from primates and human subjects. Keywords = aging Keywords = muscle cell biopsy Keywords = myotubes Keywords = glucose Keywords: time-course
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Project description:Aging is a complex process associated with multiple events that lead to the decline in stem cell number and function. However, the relationship between these events and their initiation in biological systems remains ambiguous. Here, we investigate the effects of sustained, low-grade systemic inflammation on muscle stem cells (MuSCs) during aging. We show that the slow rise in inflammation during aging causes long-lasting epigenetic remodeling in MuSCs, leading to premature exit of quiescence followed by rapid ferroptotic cell death. The elevation of circulating cytokines results in erosion of histone H4 lysine 20 methylation, fine-tuning of the MuSC transcriptome for future injury response that resembles the Galert state. Prolonged exposure to inflammatory signals during aging results in the loss of H4K20me1 maintenance by lysine methyltransferase 5a (Kmt5a), leading to a disruption of key transcriptional programs required to preserve MuSC quiescence and survival. Mechanistically, we established that Kmt5a genetic deletion prematurely activates MuSC through Notch signaling. Activated cells cannot cycle properly as they display aberrant iron metabolism and repressed Gpx4, resulting in the accumulation of reactive oxygen species, genomic instability, lipid peroxidation, and ultimately, cell death by ferroptosis. Notably, a lifelong reduction in inflammation restores the MuSC number and function and rejuvenates MuSC iron homeostasis. Our findings demonstrates that chronic systemic inflammatory signals reprogram the MuSC epigenome into a primed state, which drives premature cell cycle re-entry and ferroptosis during aging.
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Project description:Metabolic stress and changes in nutrient levels modulate many aspects of skeletal muscle function during aging and disease. Growth factors and cytokines secreted by skeletal muscle, known as myokines, are important signaling factors but it is largely unknown whether they modulate muscle growth and differentiation in response to nutrients. Here, we find that changes in glucose levels increase the activity of the glucose-responsive transcription factor MLX, which promotes and is necessary for myoblast fusion. MLX promotes myogenesis not via an adjustment of glucose metabolism but rather by inducing the expression of several myokines, including insulin like-growth factor-2 (IGF2), whereas RNAi and dominant-negative MLX reduce IGF2 expression and block myogenesis. This phenotype is rescued by conditioned media from control muscle cells and by recombinant IGF2, which activates the myogenic kinase Akt. Importantly, MLX null mice display decreased IGF2 induction and diminished muscle regeneration in response to injury, indicating that the myogenic function of MLX is conserved in vivo. Thus, glucose is a signaling molecule that regulates myogenesis and muscle regeneration via MLX/IGF2/Akt signaling.â??The data pproided are histome H4 acetlation data for MLX DN and MLX wt samples; 3 MLX DN H4 Ac Chip seq samples , 3 Inputs, 3 MLX WT H4 Ac samples and 3 WT inputs
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Project description:Aging is a complex process associated with multiple events that lead to the decline in stem cell number and function. However, the relationship between these events and their initiation in biological systems remains ambiguous. Here, we investigate the effects of sustained, low-grade systemic inflammation on muscle stem cells (MuSCs) during aging. We show that the slow rise in inflammation during aging causes long-lasting epigenetic remodeling in MuSCs, leading to premature exit of quiescence followed by rapid ferroptotic cell death. The elevation of circulating cytokines results in erosion of histone H4 lysine 20 methylation, fine-tuning of the MuSC transcriptome for future injury response that resembles the Galert state. Prolonged exposure to inflammatory signals during aging results in the loss of H4K20me1 maintenance by lysine methyltransferase 5a (Kmt5a), leading to a disruption of key transcriptional programs required to preserve MuSC quiescence and survival. Mechanistically, we established that Kmt5a genetic deletion prematurely activates MuSC through Notch signaling. Activated cells cannot cycle properly as they display aberrant iron metabolism and repressed Gpx4, resulting in the accumulation of reactive oxygen species, genomic instability, lipid peroxidation, and ultimately, cell death by ferroptosis. Notably, a lifelong reduction in inflammation restores the MuSC number and function and rejuvenates MuSC iron homeostasis. Our findings demonstrates that chronic systemic inflammatory signals reprogram the MuSC epigenome into a primed state, which drives premature cell cycle re-entry and ferroptosis during aging.
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