Similar Datasets
Project description:Healthy human skeletal muscle samples were processed and analyzed to infer age associated skeletal muscle changes.
2020-04-07 | GSE129643 | GEO
Project description:Skeletal Muscle Transcriptome in Healthy Aging
| PRJNA690800 | ENA
Project description:The age-related loss of skeletal muscle mass and function (sarcopenia) is one of the most dramatic changes affecting the human body. A clear understanding of the mechanisms involved is thus of paramount importance in ensuring quality of life in the old age. Most previous studies of sarcopenia in human investigated chronological aging, as they relied on comparisons between young and old subjects. Notably, no previous study has taken into consideration inter-individual differences (biological aging) in prevalence of sarcopenia. To obtain an integrative view of muscle biological aging our project uses a single biopsy from 72 well-phenotyped 80 years healthy subjects with different muscle loss/gain (PROOF cohort), to provide an extended characterization of the muscle tissue, including microstructural and omic analyses.
2024-05-02 | GSE174106 | GEO
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
2007-07-16 | GSE8479 | GEO
Project description:Skeletal muscle aging is a major causative factor for disability and frailty in the elderly. Recent theories about the origins of the progressive impairment of skeletal muscle with aging emphasize a disequilibrium between damage and repair. Macrophages participate in muscle tissue repair first as pro-inflammatory M1 subtype and then as M2 anti-inflammatory subtype. However, information on macrophage presence in skeletal muscle is still sporadic and the effect of aging on different phenotypes remains unknown. In this study, we sought to characterize the polarization status of macrophages human skeletal muscle at different ages. We found that most macrophages in human skeletal muscle are M2, and that this number increased with advancing age. On the contrary, M1 macrophages decline with aging, making the total number of macrophages invariant with older age. Notably, M2 macrophages co-localized with increasing intermuscular adipose tissue (IMAT) in aging skeletal muscle. The mouse strain BALB/c, intrinsically M2-prone, showed increased IMAT and regenerating myofibers in skeletal muscle, accompanied by elevated expression of adipocyte markers and M2 cytokines. Collectively, we report that polarization of macrophages to the major M2 subtype is associated with IMAT, and propose that increased M2 in aged skeletal muscle may reflect active repair of aging-associated muscle damage.
2022-01-01 | GSE125481 | GEO
Project description:Human skeletal muscle was obtained from five individuals: Two hyperglycaemic type 2 diabetics, one diabetic subjects with normal fasting glucose and two healthy control subjects matched for age and BMI.
2007-12-10 | E-MEXP-1270 | biostudies-arrayexpress
Project description:With advancing age, human muscle loses strength and function, but the molecular causes of these losses are unknown. Skeletal muscle shows an age-dependent decline in the levels of different proteins, but whether such decline is associated with reduced translation has not been studied. To address this gap of knowledge, we used the technique of ribosome profiling to study translation in muscle from middle-aged and old individuals. Using ribosome occupancy as a measure of translation status, several mRNAs showed differential translation with age. Older age was associated with lower translation of myosin and titin isoforms and more broadly with the translation of proteins involved in oxidative phosphorylation encoded by the mitochondrial genome. Based on our findings, we propose that mitochondrial proteins are less translated in old skeletal muscle.
2021-03-08 | GSE152554 | GEO
Project description:With advancing age, human muscle loses strength and function, but the molecular causes of these losses are unknown. Skeletal muscle shows an age-dependent decline in the levels of different proteins, but whether such decline is associated with reduced translation has not been studied. To address this gap of knowledge, we used the technique of ribosome profiling to study translation in muscle from middle-aged and old individuals. Using ribosome occupancy as a measure of translation status, several mRNAs showed differential translation with age. Older age was associated with lower translation of myosin and titin isoforms and more broadly with the translation of proteins involved in oxidative phosphorylation encoded by the mitochondrial genome. Based on our findings, we propose that mitochondrial proteins are less translated in old skeletal muscle.
2021-03-08 | GSE152556 | GEO
Project description:Both aging and physical activity can influence the amount of connective tissue in skeletal muscle, but the impact of these upon specific extracellular matrix (ECM) proteins in skeletal muscle is unknown. We investigated the proteome profile of connective tissue in skeletal muscle by label-free proteomic analysis of on cellular protein-depleted extracts from lateral gastrocnemius muscle of old (22-23 months old) and middle-aged mice (11 months old) subjected to three different levels of regular physical activity for 10 weeks (high resistance wheel running, low resistance wheel running or sedentary controls). We hypothesized that aging is correlated with increased amount of connective tissue proteins in skeletal muscle, and that regular physical activity can counteract these age-related changes. We found that dominating cellular proteins were diminished in the urea/thiourea extract, which was therefore used for proteomics. Proteomic analysis identified 482 proteins and showed enrichment for ECM proteins. Statistical analysis revealed that the abundances of 86 proteins were changed with age. Twenty-three of these differentially abundant proteins were identified as structural ECM proteins (e.g., collagens and laminins) and all of these were significantly more abundant with aging. No significant effect of training or interaction between training and advance in age was found for any proteins. Finally, we found a lower protein concentration in the urea/thiourea extracts from the old compared to middle-aged mice. These findings indicate that intramuscular connective tissue alters its protein content with age but is unaffected by training.
2023-04-27 | PXD036532 | Pride
Project description:Utilizing glycerol intramuscular injections in M. musculus provide a models of skeletal muscle damage followed by skeletal muscle regeneration. In particular, glycerol-induced muscle injury triggers accute activation of skeletal muscle stem cells, called satellite cells. However, aging dramatically impairs the regenerative capacity of satellite cells. We characterized genome-wide expression profiles of young and old satellite cells in the non-proliferative and activated state, freshly isolated to non-injured or damaged muscles, respectively. Our goal was to uncover new regulatory signaling specific to satellite cells entry into the activation and myogenic program that are affected with age.
2016-07-04 | GSE81096 | GEO