Age-related changes in human skeletal muscle transcriptome and proteome are more affected by chronic inflammation and physical inactivity than primary aging
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ABSTRACT:
PROVIDER: PRJNA1011971 | ENA |
REPOSITORIES: ENA
Dataset's files
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| SRR25879400.fastq.gz | Fastqsanger.gz | |||
| SRR25879401.fastq.gz | Fastqsanger.gz | |||
| SRR25879402.fastq.gz | Fastqsanger.gz | |||
| SRR25879403.fastq.gz | Fastqsanger.gz | |||
| SRR25879404.fastq.gz | Fastqsanger.gz |
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Project description:Evaluation of the influence of primary and secondary aging on the manifestation of molecular and cellular hallmarks of aging is a challenging and currently unresolved issue. Our study represents the first demonstration of the distinct role of primary aging and both chronic inflammation and physical inactivity – the most important drivers of secondary aging, in the regulation of transcriptomic and proteomic profiles in human skeletal muscle. To achieve this purpose, young healthy people (n=15), young (n=8) and older (n=37) patients with knee/hip osteoarthritis, a model to study the effect of long-term inactivity and chronic inflammation on the vastus lateralis muscle, were included in the study. It was revealed that widespread and substantial age-related changes in gene expression (~4,000 genes regulating mitochondrial function, proteostasis, cell membrane, secretory and immune response) were related to the long-term physical inactivity and chronic inflammation rather than primary aging. Primary aging contributed mainly to the regulation of genes (~200) encoding nuclear proteins (regulators of DNA repair, RNA processing, and transcription), mitochondrial proteins (genes encoding respiratory enzymes, mitochondrial complex assembly factors, regulators of cristae formation and mitochondrial reactive oxygen species production), as well as regulators of proteostasis. It was found that proteins associated with aging were regulated mainly at the post-transcriptional level. The set of putative primary aging genes and their potential transcriptional regulators can be used as a resource for further targeted studies investigating the role of individual genes and related transcription factors in the emergence of a senescent cell phenotype.
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Project description:Global gene expression of the rat soleus muscle was assessed with microarrays after 12 hrs of physical inactivity and also after 12 hours of physical inactivity immediately followed by 2 hrs treadmill walking and compared to normally caged rats with voluntary standing and intermittent cage movements. Keywords: between group design
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Project description:Global gene expression of the rat soleus muscle was assessed with microarrays after 12 hrs of physical inactivity and also after 12 hours of physical inactivity immediately followed by 2 hrs treadmill walking and compared to normally caged rats with voluntary standing and intermittent cage movements. Experiment Overall Design: Rats were either prevented from standing on the their hindlimbs for 12 hrs or were prevented from standing on the their hindlimbs for 12 hrs and then immediately engaged in 2 hours treadmill walking and compared to caged rats with normal standing/ambulatory activity. RNA was extracted from soleus muscles and each array represents the pooling of the RNA from the soleus of 8-10 different rats.
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Project description:Global gene expression of the rat soleus muscle was assessed with microarrays after 11 days of intermittent physical inactivity (10 hr/day) and compared to normally caged rats with voluntary standing and intermittent cage movements. Keywords: between group design
2006-07-04 | GSE5217 | GEO
Project description:Global gene expression of the rat soleus muscle was assessed with microarrays after 11 days of intermittent physical inactivity (10 hr/day) and compared to normally caged rats with voluntary standing and intermittent cage movements. Experiment Overall Design: Rats were prevented from standing on the their hindlimbs for 10 hrs/day for 11 days and compared to caged rats with normal standing/ambulatory activity. RNA was extracted from soleus muscles and each array represents the pooling of the RNA from the soleus of 4-5 different rats.
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Project description:Insufficient physical activity is associated with increased relative risk of cardiometabolic disease and is an independent risk factor for mortality. Experimentally reducing physical activity rapidly induces insulin resistance, impairs glucose handling, and drives metabolic inflexibility. These adaptations manifest during the early stages of physical inactivity, even when energy balance is maintained, suggesting that inactivity-mediated metabolic reprogramming is an early event that precedes changes in body composition. To identify mechanisms that promote metabolic adaptations associated with physical inactivity, we developed a mouse model of physical activity reduction that permits the study of inactivity in animals prior to the onset of overt changes in body composition. Adult mice were randomized into three groups: an inactive control group (standard housing), an active control group (treadmill running for 6-weeks), and an activity reduction group (treadmill running for 4-weeks, followed by 2-weeks of inactivity). Transcriptional profiling of gastrocnemius muscle was performed.
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2010-09-21 | E-GEOD-24215 | biostudies-arrayexpress
Project description:Rationale: Physical inactivity is a risk factor for insulin resistance. We examined the effect of nine days of bed rest on basal and insulin stimulated expression of genes potentially involved in insulin action by applying hypothesis-generating microarray in parallel with candidate gene real-time PCR approaches in 20 healthy, young men. Furthermore, we investigated whether bed rest affected DNA methylation in the promoter region of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A) gene. Subjects were re-examined after four weeks of retraining. Findings: Bed rest induced insulin resistance and altered the expression of more than 4,500 genes. These changes were only partly normalized after four weeks of retraining. Pathway analyses revealed significant down-regulation of 34 pathways, predominantly those of genes associated with mitochondrial function including PPARGC1A. Despite induction of insulin resistance, bed rest resulted in a paradoxically increased response to acute insulin in the general expression of genes, particularly those involved in inflammation and endoplasmatic reticulum (ER) stress. Furthermore, bed rest changed gene expressions of several insulin resistance and diabetes candidate genes. We also observed a trend toward increased PPARGC1A DNA methylation after bed rest. Conclusions: Impaired expression of PPARGC1A and other genes involved in mitochondrial function as well as a paradoxically increased response to insulin of genes involved in inflammation and ER stress may contribute to the development of insulin resistance induced by bed rest. Lack of complete normalization of changes after four weeks of exercise retraining underscores the importance of maintaining a minimum of daily physical activity.
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Project description:Skeletal muscle plasticity is imperative for functional adaptation to changing demands. Although a great deal is known about the structural and functional plasticity of healthy skeletal muscle, far less is known about plasticity in diseased muscle. Here, we created an experimental design to better understand how dystrophin-deficient zebrafish muscle responds to inactivity versus activity. We tested two inactivity paradigms, intermittent versus extended inactivity, and found that extended inactivity, defined as 72 hours in low-dose tricaine, worsens muscle structure and decreases survival. Strikingly, extended inactivity followed by a single session of neuromuscular electrical stimulation (NMES) further worsens muscle structure and obliterates its ability to regenerate. Next, we tested four unique NMES paradigms that varied in their frequency and voltage, and found that each NMES paradigm differentially affected muscle structure, function, and survival. However, one NMES paradigm, which we refer to as endurance NMES, improved all three components of muscle health. Accompanying these improvements, we observed increased sarcomere lengths as well as larger surface areas, volumes, and filament indices of muscle nuclei. Additionally, time-lapse imaging reveals less degeneration and improved regeneration of the fast-twitch muscle fibers. RNAseq analysis highlights two potential mechanisms, one in which gene expression levels are returned to wild-type levels as well as remodeling of the extracellular matrix. Collectively, these data provide a new methodology with which to study neuromuscular plasticity in healthy versus diseased muscle. In addition, our data clearly indicate that, at least in the zebrafish model, NMES is beneficial whereas inactivity is deleterious for dystrophic muscle.
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