Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA101511 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Inadequate dietary protein intake causes adverse changes in the morphology and function of skeletal muscle. These changes may be reflected in early alterations in muscle mRNA levels. Microarray analysis was used to assess whether inadequate protein intake differentially affects skeletal muscle transcript levels and expression profiles in older adults. Keywords: dietary intake response
2007-07-11 | GSE8441 | GEO
Project description:Inadequate dietary protein intake causes adverse changes in the morphology and function of skeletal muscle. These changes may be reflected in early alterations in muscle mRNA levels. Microarray analysis was used to assess whether inadequate protein intake differentially affects skeletal muscle transcript levels and expression profiles in older adults. Experiment Overall Design: 11 older males and females (aged 55-80 y) consumed controlled diets that contained 1.2 g proteinâ¢kg-1â¢d-1 (adequate protein) for one wk and then 0.5 g proteinâ¢kg-1â¢d-1 (inadequate protein; IP group; n=11) for a second wk. RNA was isolated from fasting-state vastus lateralis biopsies obtained at the end of each period and the transcript levels were determined using the Affymetrix U133A array
2008-06-16 | E-GEOD-8441 | biostudies-arrayexpress
Project description:The skeletal muscle transcript profile reflects responses to inadequate protein intake in younger and older males
| PRJNA103159 | ENA
Project description:Inadequate protein intake initiates an accommodative response with adverse changes in skeletal muscle function and structure. mRNA level changes due to short-term inadequate dietary protein might be an early indicator of accommodation. The aims of this study were to assess the effects of dietary protein and the diet-by-age interaction on the skeletal muscle transcript profile. Self-organizing maps were used to determine expression patterns across protein trials. 958 transcripts were differentially expressed (P<0.05) with diet and 853 had a diet-by-age interaction (P<0.05) using ANOVA. The results for diet alone revealed that P63 was associated with up-regulation of transcripts related to ubiquitin-dependent protein catabolism and muscle contraction and P63 and P94 resulted in up-regulation of transcripts related to apoptosis and down-regulation of transcripts related to cell differentiation; muscle and organ development; extracellular space; and responses to stimuli and stress. The diet-by-age expression patterns demonstrated that across the three protein trials transcripts related to protein metabolism were affected by age. Changes in skeletal muscle mRNA levels in the younger and older males to protein intake near or below the RDA are indicative of an early accommodative response. 5052 transcripts were determined as differentially expressed (P<0.05) between the younger and older males, of which 2556 met the False Discovery Rate correction (P=0.0081). The age-related changes in the transcript profile were consistent with aging skeletal muscle phenotypes including; mitochondrial dysfunction (UP- and DOWN-regulation), RNA splicing (UP), oxidative stress (UP), apoptosis (UP), and energy metabolism (DOWN). Experiment Overall Design: 22 healthy free-living younger (21-43 y, n=12) and older (63-79 y, n=10) males completed three controlled feeding trials with protein intakes of 63% (P63: 0.50 g/kg), 94% (P94: 0.75 g/kg), and 125% (P125: 1.00 g/kg) of the recommended dietary allowance (RDA). A fasting state vastus lateralis biopsy was taken from the dominant leg of each subject on day 12 of each trial following an overnight fast. Total RNA was isolated from the muscle samples using Tri-Reagent and the manufacture's protocol.
2008-10-26 | E-GEOD-9419 | biostudies-arrayexpress
Project description:Inadequate protein intake initiates an accommodative response with adverse changes in skeletal muscle function and structure. mRNA level changes due to short-term inadequate dietary protein might be an early indicator of accommodation. The aims of this study were to assess the effects of dietary protein and the diet-by-age interaction on the skeletal muscle transcript profile. Self-organizing maps were used to determine expression patterns across protein trials. 958 transcripts were differentially expressed (P<0.05) with diet and 853 had a diet-by-age interaction (P<0.05) using ANOVA. The results for diet alone revealed that P63 was associated with up-regulation of transcripts related to ubiquitin-dependent protein catabolism and muscle contraction and P63 and P94 resulted in up-regulation of transcripts related to apoptosis and down-regulation of transcripts related to cell differentiation; muscle and organ development; extracellular space; and responses to stimuli and stress. The diet-by-age expression patterns demonstrated that across the three protein trials transcripts related to protein metabolism were affected by age. Changes in skeletal muscle mRNA levels in the younger and older males to protein intake near or below the RDA are indicative of an early accommodative response. 5052 transcripts were determined as differentially expressed (P<0.05) between the younger and older males, of which 2556 met the False Discovery Rate correction (P=0.0081). The age-related changes in the transcript profile were consistent with aging skeletal muscle phenotypes including; mitochondrial dysfunction (UP- and DOWN-regulation), RNA splicing (UP), oxidative stress (UP), apoptosis (UP), and energy metabolism (DOWN). Keywords: Age and dietary protein response
2008-09-22 | GSE9419 | GEO
Project description:Transcriptomics analysis of skeletal muscle in humans with heart failure
2025-01-16 | E-MTAB-8531 | ExpressionAtlas
Project description:A transcriptomic study was performed on muscle, liver and brain a group of 3 embryos with a mutation in ADCK2 gene (controls being wild-type embryos from the same litter). Haploinsufficiency of ADCK2 leads to reduced mitochondrial coenzyme Q (CoQ) levels in skeletal muscle, resulting in mitochondrial myopathy, alterations in fatty acid beta-oxidation and physical incapacity in both humans and mice at adult stage (PMID: 31480808). Adck2 heterozygous mice exhibit defects from the embryonic development stage, particularly in skeletal muscle. Prenatal administration of CoQ10 can mitigate the defects observed during embryonic development. Ablation of Adck2 affects postnatal myogenesis, with more severe consequences in older mice. Consequently, heterozygous Adck2 mice display accelerated muscle wasting associated with ageing. Prenatal administration of CoQ10 can prevent these defects.
2024-12-19 | GSE253654 | GEO
Project description:The skeletal muscle system plays an important role in the independence of older adults. In this study we examine differences in the skeletal muscle transcriptome between healthy young and older subjects and (pre‐)frail older adults. Additionally, we examine the effect of resistance‐type exercise training on the muscle transcriptome in healthy older subjects and (pre‐)frail older adults. Baseline transcriptome profiles were measured in muscle biopsies collected from 53 young, 73 healthy older subjects, and 61 frail older subjects. Follow‐up samples from these frail older subjects (31 samples) and healthy older subjects (41 samples) were collected after 6 months of progressive resistance‐type exercise training. Frail older subjects trained twice per week and the healthy older subjects trained three times per week. At baseline genes related to mitochondrial function and energy metabolism were differentially expressed between older and young subjects, as well as between healthy and frail older subjects. Three hundred seven genes were differentially expressed after training in both groups. Training affected expression levels of genes related to extracellular matrix, glucose metabolism, and vascularization. Expression of genes that were modulated by exercise training was indicative of muscle strength at baseline. Genes that strongly correlated with strength belonged to the protocadherin gamma gene cluster (r = −0.73). Our data suggest significant remaining plasticity of ageing skeletal muscle to adapt to resistance‐type exercise training. Some age‐related changes in skeletal muscle gene expression appear to be partially reversed by prolonged resistance‐type exercise training. The protocadherin gamma gene cluster may be related to muscle denervation and re‐innervation in ageing muscle.
2018-07-24 | GSE117525 | GEO
Project description:The loss of skeletal muscle mass during aging is a significant health concern linked to adverse outcomes in older individuals. Understanding the molecular basis of age-related muscle loss is crucial for developing strategies to prevent or reverse this debilitating condition. Long non-coding RNAs (lncRNAs) are a largely uncharacterized class of biomolecules that have been implicated in cellular homeostasis and dysfunction across a wide variety of tissues and cell types. To identify lncRNAs that might contribute to skeletal muscle aging we screened for lncRNAs whose expression was altered in vastus lateralis muscle from older compared to young adults. We identified FRAIL1 as an aging-induced lncRNA with high abundance in human skeletal muscle. In a cohort of healthy young and older adults, skeletal muscle FRAIL1 was most strongly expressed in older females and negatively associated with measures of muscle strength and mass. Forced expression of FRAIL1 in mouse tibialis anterior muscle elicits a dose-dependent reduction in skeletal muscle fiber size that is independent of changes in muscle fiber type. Furthermore, this reduction in muscle size is dependent on an intact region of FRAIL1 that is highly conserved across non-human primates. Unbiased transcriptional and proteomic profiling of the effects of FRAIL1 expression in mouse skeletal muscle revealed widespread changes in mRNA and protein abundance that recapitulate age-related changes in pathways and processes that are known to be altered in aging skeletal muscle. Taken together, these findings shed light on the intricate molecular mechanisms underlying skeletal muscle aging and implicate FRAIL1 in the reduction of muscle mass during this process.
2024-02-24 | GSE249356 | GEO
Project description:Background: Periods of inactivity experienced by older adults induce nutrient anabolic resistance creating a cascade of skeletal muscle transcriptional and translational aberrations contributing to muscle dysfunction. Objective: To identify how inactivity alters leucine-stimulated translation of molecules and pathways within the skeletal muscle of older adults.
2020-12-06 | GSE162730 | GEO