Changes in gene expression after mechanical loading with and without satellite cell.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE153542 | GEO | 2021/07/12
REPOSITORIES: GEO
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Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Overload like resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. Using compensatory hypertrophy in plantaris muscles, we isolated MuSCs from plantaris muscles 4 days after surgery. Control MuSCs were also prepared from sham plantaris muscles.
2019-09-23 | GSE135903 | GEO
Project description:Global gene expression patterns were determined from microarray results from sham surgery or following 1 week of plantaris muscle hypertrophy induced by synergist ablation in young adult Pax7-DTA mice (4 months). Vehicle treated mice have their full complement of satellite cells; tamoxifen treated mice have had their satellite cells genetically depleted through Cre-loxP technology After sham surgery or 1 week of overload, Affymetrix chips (mouse430_2.0) were used with 1 µg of total RNA derived from a pooled sample of the right and left plantaris muscles from 11 animals.
2014-02-20 | E-GEOD-52597 | biostudies-arrayexpress
Project description:Cachexia is a systemic metabolic syndrome characterized by loss of fat and skeletal muscle mass in chronic wasting diseases such as cancer. The regulation of cellular protein synthesis in response to workload in skeletal muscle is generally blunted in cancer cachexia; however, the precise molecular regulation is largely unknown. In this study, to examine the molecular mechanism of skeletal muscle protein metabolism in cancer cachexia, we analyzed comprehensive gene expression in skeletal muscle using microarrays. CD2F1 mice (male, 7 weeks old) were subcutaneously transplanted (1*10^6 cells per mouse) with a mouse colon cancer-derived cell line (C26) as a model of cancer cachexia. Functional overload of the plantaris muscle by synergist ablation was performed at the 2nd week, and the plantaris muscle was sampled at the 4th week of cancer transplantation. The hypertrophy of skeletal muscle (increased skeletal muscle weight/protein synthesis efficiency and activation of mTOR signaling) associated with compensatory overload was significantly suppressed with the cancer cachexia. Gene expression profiling and pathway analysis by microarray showed that resistance to muscle protein synthesis associated with cancer cachexia was induced by downregulation of insulin-like growth factor-1. These observations show that cancer cachexia induces resistance to muscle protein synthesis, which could be a potential factor inhibiting the adaptation of skeletal muscle growth to physical exercise.
2021-10-15 | GSE185934 | GEO
Project description:Skeletal muscle adaptation to external stimuli, such as regeneration following injury and hypertrophy in response to resistance exercise, are blunted with advanced age. The accumulation of senescent cells, along with defects in myogenic progenitor cell (MPC) proliferation, have been strongly linked as contributing factors to age-associated impairment in muscle adaptation. p53 plays an integral role in all these processes, as upregulation of p53 causes apoptosis in senescent cells and prevents mitotic catastrophe in MPCs from old mice. The goal of this study was to determine if a novel pharmaceutical agent (BI01), which functions by upregulating p53 through inhibition of binding to MDM2, the primary p53 regulatory protein, improves muscle regeneration and hypertrophy in old mice. BI01 effectively reduced the number of senescent cells in vitro but had no effect on MPC survival or proliferation at a comparable dose. Following repeated oral gavage with 2 mg/kg of BI01 (OS) or vehicle (OV), old mice (24 months) underwent unilateral BaCl2 injury in the tibialis anterior (TA) muscle, with PBS injections serving as controls. After 7 days, satellite cell number was higher in the TA of OS compared to OV mice, as was the expression of genes involved in ATP production. By 35 days, old mice treated with BI01 displayed reduced senescent cell burden, enhanced regeneration (higher muscle mass and fiber cross-sectional area) and restoration of muscle function relative to OV mice. To examine the impact of 2 mg/kg BI01 on muscle hypertrophy, the plantaris muscle was subjected to 28 days of mechanical overload (MOV) in OS and OV mice. In response to MOV, OS mice had larger plantaris muscles and muscle fibers than OV mice, particularly type 2b + x fibers, associated with reduced senescent cells. Together our data show that BI01 is an effective senolytic agent that may also augment muscle metabolism to enhance muscle regeneration and hypertrophy in old mice.
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Project description:MicroRNAs (miRNAs) are small, non-coding RNAs that play a critical role in regulating gene expression post-transcriptionally. Skeletal muscle-specific miRNAs, including miR-1, are important for skeletal muscle development and maintenance. In response to mechanical loading, skeletal muscle levels of miR-1 decrease by approximately 50%, suggesting a potential involvement in muscle hypertrophy. In the current investigation, we hypothesized that a reduction of miR-1 levels in response to mechanical loading would be necessary for skeletal muscle growth to occur. By significantly elevating miR-1 levels during the hypertrophic process via lentiviral delivery, we observed a blunted growth response in the plantaris muscle subjected to synergist ablation. A deeper RNA-based integrative analysis (transcriptomics and RNA eCLIP) indicates that miR-1 inhibits the expression of Itm2a and Melusin, two membrane-related proteins. While their exact mechanism in muscle hypertrophy is yet to be identified, our results suggest that miR-1-regulated membrane proteins are important for skeletal muscle hypertrophy.
2025-01-13 | GSE265982 | GEO
Project description:MicroRNAs (miRNAs) are small, non-coding RNAs that play a critical role in regulating gene expression post-transcriptionally. Skeletal muscle-specific miRNAs, including miR-1, are important for skeletal muscle development and maintenance. In response to mechanical loading, skeletal muscle levels of miR-1 decrease by approximately 50%, suggesting a potential involvement in muscle hypertrophy. In the current investigation, we hypothesized that a reduction of miR-1 levels in response to mechanical loading would be necessary for skeletal muscle growth to occur. By significantly elevating miR-1 levels during the hypertrophic process via lentiviral delivery, we observed a blunted growth response in the plantaris muscle subjected to synergist ablation. A deeper RNA-based integrative analysis (transcriptomics and RNA eCLIP) indicates that miR-1 inhibits the expression of Itm2a and Melusin, two membrane-related proteins. While their exact mechanism in muscle hypertrophy is yet to be identified, our results suggest that miR-1-regulated membrane proteins are important for skeletal muscle hypertrophy.
2025-01-13 | GSE265946 | GEO
Project description:Global gene expression patterns were determined from microarray results from sham surgery or following 1 week of plantaris muscle hypertrophy induced by synergist ablation in young adult Pax7-DTA mice (4 months). Vehicle treated mice have their full complement of satellite cells; tamoxifen treated mice have had their satellite cells genetically depleted through Cre-loxP technology
2014-02-20 | GSE52597 | GEO
Project description:With aging, skeletal muscle plasticity is attenuated in response to exercise. Here, we report that senescent cells, identified using senescence markers senescence-associated β-Galactosidase (SA β-Gal) and p21 are very infrequent in resting muscle but emerge approximately two-weeks after a bout of resistance exercise in humans. We hypothesized that these cells contribute to blunted hypertrophic potential in old age. Using synergist ablation-induced mechanical overload of the plantaris muscle to model resistance training in adult (5-6 month) and old (23-24 month) male C57BL/6J mice, we found increased senescent cells in both age groups during hypertrophy. Consistent with the human data, there were negligible senescent cells in adult and old sham controls, but old mice had significantly more senescent cells 7- and 14-days following overload relative to young. Old mice had blunted whole muscle hypertrophy when compared to adult mice, along with smaller muscle fibers, specifically glycolytic Type 2x+2b fibers. To ablate senescent cells using a hit-and-run approach, old mice were treated with vehicle or a senolytic cocktail consisting of 5 mg/kg dasatinib and 50 mg/kg quercetin (D+Q) on day 7 and 10 during 14-days of overload; control mice underwent sham surgery with or without senolytic treatment. Old mice given D+Q had larger muscles and muscle fibers after 14 days of overload, fewer senescent cells when compared to vehicle-treated old mice, and changes in the expression of genes (i.e., Igf1, Ddit4, Mmp14) that are associated with hypertrophic growth . Our data collectively show that senescent cells emerge in human and mouse skeletal muscle following a hypertrophic stimulus, and that D+Q improves muscle growth in old mice.
2022-05-29 | GSE195707 | GEO
Project description:Divergent skeletal muscle phenotypes result from chronic resistance-type- versus endurance-type contraction, reflecting the principle of training specificity. However, it is unclear whether there is a common set of genetic factors that influence skeletal muscle adaptation to different modes of training. Female rats were obtained from out-bred lines selectively bred from high responders to endurance training (HRT) or low responders to endurance training (LRT; n=6/group; generation 19). Both groups underwent 14 d of synergist ablation to induce functional overload of the plantaris muscle prior to comparison to non-overload controls of the same genotype. RNA sequencing was performed to identify Gene Ontology Biological Processes with differential (LRT vs HRT) gene set enrichment. Running distance, determined well in advance of synergist ablation, increased in response to aerobic training in HRT but not LRT (65 ±26% versus -6 ±18%, respectively, mean ±SD, p<0.0001). The hypertrophy response to functional overload was attenuated in LRT versus HRT (20.1 ±5.6% versus 41.6 ±16.1%, respectively, P = 0.015). There were between-group differences in the magnitude of response of 96 upregulated- and 101 downregulated pathways. A further 27 pathways showed contrasting upregulation or downregulation in LRT versus HRT in response to functional overload. In conclusion, low responders to aerobic endurance training were also low responders for compensatory hypertrophy, and attenuated hypertrophy was associated with differential gene expression. Thus, our findings suggest that genetic factors that underpin aerobic training maladaptation may also dysregulate the transcriptional activity of biological processes that contribute to adaptation to mechanical overload.
2020-12-31 | GSE156724 | GEO
Project description:Skeletal muscle specific overexpression of miRNA-1 impairs mechanical overload-induced skeletal muscle hypertrophy
| PRJNA1105018 | ENA