Skeletal muscle specific overexpression of miRNA-1 impairs mechanical overload-induced skeletal muscle hypertrophy [RNA-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1105087 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28816702_1.fastq.gz | Fastqsanger.gz | |||
| SRR28816702_2.fastq.gz | Fastqsanger.gz | |||
| SRR28816703_1.fastq.gz | Fastqsanger.gz | |||
| SRR28816703_2.fastq.gz | Fastqsanger.gz | |||
| SRR28816704_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Skeletal muscle specific overexpression of miRNA-1 impairs mechanical overload-induced skeletal muscle hypertrophy
| PRJNA1105018 | ENA
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: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:Skeletal muscle is a plastic tissue, adapting to different stimuli. Mechanical overload causes muscle hypertrophy and substantial changes in gene expression. We perform a time course analysis following synergistic ablation surgery to induce compensatory hypertrophy in the plantaris muscle in satellite cell depleted mice and wild-type mice. Microarray was used to determine the different expressed genes in skeletal muscle with or without satellite cell following mechanical overload.
2021-07-12 | GSE153542 | GEO
Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy. We applied TAC to wild type and MAFbx KO mice, and extracted total RNA one week after the surgery. The gene expression profiles were examined by Affymetrix Mouse Gene ST Array.
2011-05-01 | E-GEOD-24372 | biostudies-arrayexpress
Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy.
2011-05-01 | GSE24372 | 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:How regular physical activity is able to improve health remains poorly understood, but release of substances from skeletal muscle following exercise is one proposed mechanism. Here we describe a novel mechanism through which physical activity initiates extracellular vesicle (EV)-mediated communication between skeletal muscle and adipose tissue causing increased adipocyte lipolysis as a result of enhanced catecholamine sensitivity. In response to a hypertrophic stimulus induced by mechanical overload (MOV), skeletal muscle released EVs containing muscle-specific miR-1 which were preferentially taken up by epididymal white adipose tissue (eWAT) and were associated with elevated adrenergic signaling and lipolysis. Inhibiting EV release by GW4869 treatment prevented the MOV-induced increase in eWAT miR-1 abundance and expression of lipolytic factors. miR-1 was shown to induce adrenergic receptor beta β3 (Adrβ3) expression in adipocytes by targeting transcription factor AP-2, alpha (Tfap2α, a known repressor of Adrβ3 expression. Ex vivo experiments showed enhanced catecholamine sensitivity and elevated fatty acid oxidation in eWAT following MOV. Following a bout of resistance exercise in humans, skeletal muscle miR-1 expression was decreased with a concomitant increase in EV miR-1 abundance, suggesting that a skeletal muscle-adipose tissue axis is operative in humans. Altogether, our highly novel findings demonstrate that skeletal muscle promotes metabolic adaptations in adipose tissue in response to MOV via EV-mediated delivery of miR-1.
2021-05-26 | GSE150162 | 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: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