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ABSTRACT:
PROVIDER: PRJNA1103358 | ENA |
REPOSITORIES: ENA
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Project description:Microbiome research related to muscle strength improvement
| PRJEB85118 | ENA
Project description:The loss of muscle size, strength and quality with ageing, is a major determinant of morbidity and mortality in the elderly. The regulatory pathways that impact on the muscle phenotype include the translational regulation maintained by microRNAs (miRNA). Yet the miRNAs that are expressed in human skeletal muscle and whose expression levels correlate to muscle size, strength and quality are unknown. Here we used next-generation sequencing to characterise the expression profile of miRNAs in the m. vastus lateralis obtained by biopsy from middle-aged males (n=48; 50.0±4.3 years). Isokinetic strength testing and mid-thigh computed tomography was undertaken for muscle phenotype analysis. miR-486-5p accounted for 21% of the total miR sequence reads, with miR-10b-5p, miR-133a-3p, and miR-22-3p accounting for a further 15%, 12% and 10% respectively. Isokinetic knee extension strength and muscle cross-sectional area were positively correlated with miR-100-5p, miR-99b-5p and miR-191-5p expression. Whilst muscle attenuation, reflective of myofiber lipid content was negatively correlated to let-7f-5p, miR-30d-5p and miR-125b-5p expression. In-silico analysis implicates miRNAs related to strength and muscle size in the regulation of mammalian target of rapamycin, whist miRNAs related to muscle attenuation may have potential roles controlling the transforming growth factor- β/SMAD3 pathway which regulated fibrosis, adipogenesis and lipid accumulation.
2018-01-10 | GSE103635 | GEO
Project description:This experiment was conducted to identify the mitochondrial protein changes in the presence and absence of LONP1 in skeletal muscle. The following abstract from the submitted manuscript describes the major findings of this work.Disuse-associated loss of muscle LONP1 impairs mitochondrial quality and causes reduced skeletal muscle mass and strength. Zhisheng Xu, Tingting Fu, Qiqi Guo, Danxia Zhou, Wanping Sun, Zheng Zhou, Lin Liu, Liwei Xiao, Yujing Yin, Yuhuan Jia, Xin Pan, Lei Fang, Min-sheng Zhu, Wenyong Fei, Bin Lu and Zhenji Gan. Mitochondrial proteolysis is an evolutionarily conserved quality control mechanism to maintain proper mitochondrial integrity and function. However, the physiological relevance of stress-induced impaired mitochondrial protein quality remains unclear. Here, we demonstrate that LONP1, a major mitochondrial protease resides in the matrix, plays a critical role in controlling mitochondrial quality as well as skeletal muscle mass and strength in response to muscle disuse. In humans and mice, disuse-related muscle loss is associated with decreased mitochondrial LONP1 protein. Skeletal muscle-specific ablation of LONP1 in mice resulted in impaired mitochondrial protein turnover, leading to mitochondrial dysfunction. This caused reduced muscle fiber size and strength. Mechanistically, aberrant accumulation of mitochondrial-retained protein in muscle upon loss of LONP1 induces the activation of autophagy-lysosome degradation program of muscle loss. Overexpressing a mitochondrial-retained mutant ornithine transcarbamylase (ΔOTC), a known protein degraded by LONP1, in skeletal muscle induces mitochondrial dysfunction, autophagy activation, and cause muscle loss and weakness. Thus, these findings reveal a pivotal role of LONP1-dependent mitochondrial protein quality-control in safeguarding mitochondrial function and preserving skeletal muscle mass and strength, and unravel an intriguing link between mitochondrial protein quality and muscle mass maintenance during muscle disuse.
2022-01-05 | PXD029722 | Pride
Project description:We combined an experimental microbiome of 11 bacterial strains isolated from the gut of native Caenorhabditis elegans. C. elegans were maintained on the experimental microbiome, Escherichia coli OP50 (control food source), or OP50 supplemented with cell-free media (CFM) from the experimental microbiome. For each of the three feeding conditions, RNA-seq was performed for wildtype (N2) worms or transgenic worms expressing amyloid beta 1-42 in their body wall muscle (GMC101).
2022-06-23 | E-MTAB-10693 | biostudies-arrayexpress
Project description:Age-related sarcopenia is associated with a variety of changes in skeletal muscle. These changes are interrelated with each other and associated with systemic metabolism, the details of which, however, are largely unknown. Eicosapentaenoic acid (EPA) is a promising nutrient against sarcopenia and has multifaceted effects on systemic metabolism. Although several human studies have suggested that EPA supplementation protects against sarcopenia, the causal relationship of EPA supplementation and an increase of muscle strength has poor evidence in vivo. We demonstrated that aging skeletal muscle in male mice shows lower grip strength and fiber type changes, both of which can be inhibited by EPA supplementation irrespective of muscle mass alteration. We hypothesized that the aging process in skeletal muscle can be intervened by the administration of EPA, via transcriptomic changes in skeletal muscle. This analysis revealed fast-to-slow fiber type transition in aging muscle, which was partially inhibited by EPA.
2020-12-21 | GSE149307 | 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:Combining resistance and endurance exercises in a training regime (concurrent training) can impair improvements in muscle hypertrophy, strength, and power compared to resistance training alone. Here we aimed to characterize skeletal muscle transcriptomic changes following chronic concurrent training to determine whether contraction-induced gene expression may reveal molecular underpinnings explaining impaired adaptations. Eighteen young, healthy male participants underwent 12 weeks of resistance, endurance, or concurrent training. Maximal strength, aerobic capacity, and anaerobic power were assessed. Transcriptomics were performed on skeletal muscle biopsies obtained pre and post-intervention. Improvements to maximal anaerobic power are impaired with concurrent and endurance training. Gene expression related to plasma membrane structures was enriched while gene expression related to regulation of mRNA processing and protein degradation was suppressed with concurrent training. Considerable overlap of gene expression related to extracellular matrix remodeling was observed between concurrent and endurance training. Our results provide the first comprehensive comparison of unique and overlapping gene sets enriched following chronic resistance, endurance, and concurrent training, and reveals pathways that may have implications in relation to impaired adaptations when undertaking concurrent training.
2023-04-01 | GSE137832 | GEO