Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1217587 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Androgens have a strong effect against skeletal muscles to increase muscle mass and strength. However, a molecular mechanism of AR action on muscle strength is not clear. To identify the target genes of AR in skeletal muscle, we generated myofiber specific ARKO using HSA-Cre and AR flox mice (cARKO). Nine-week-old female control and cARKO mice were treated with or without DHT for 4 weeks. After euthenization, gastrocunemius muscle were collected and total RNA were extracted.
2021-03-10 | GSE152756 | GEO
Project description:The goal of this study was to identify changes in muscle gene expression that may contribute to loss of adaptability of old muscle. Muscle atrophy was induced in young adult (6-month) and old (32-month) male Brown Norway/F344 rats by two weeks of hind limb suspension (HS) and soleus muscles were analyzed by cDNA microarrays. We conclude that a cold shock response may be part of a compensatory mechanism in muscles undergoing atrophy to preserve remaining muscle mass and that RBM3 may be a therapeutic target to prevent muscle loss.
2008-07-23 | GSE12087 | GEO
Project description:As a consequence of impaired glucose or fatty acid metabolism, bioenergetic stress in skeletal muscles may trigger myopathy and rhabdomyolysis. Genetic mutations causing loss of function of the LPIN1 gene frequently lead to severe rhabdomyolysis bouts in children, though the metabolic alterations and possible therapeutic interventions remain elusive. Here, we show that lipin1 deficiency in mouse skeletal muscles is sufficient to trigger myopathy. Strikingly, muscle fibers display strong accumulation of both neutral and phospholipids. The metabolic lipid imbalance can be traced to an altered fatty acid synthesis and fatty acid oxidation, accompanied by a defect in acyl chain elongation and desaturation. As an underlying cause, we reveal a severe sarcoplasmic reticulum (SR) stress, leading to the activation of the lipogenic SREBP1c/SREBP2 factors, the accumulation of the Fgf21 cytokine, and alterations of SR-mitochondria morphology. Importantly, pharmacological treatments with the chaperone TUDCA and the fatty acid oxidation activator bezafibrate improve muscle histology and strength of lipin1 mutants. Our data reveal that SR stress and alterations in SR-mitochondria contacts are contributing factors and potential intervention targets of the myopathy associated with lipin1 deficiency.
2019-01-07 | MTBLS750 | MetaboLights
Project description:Low-intensity neuromuscular electrical stimulation (NMES) is often used as an alternative to exercise and high-intensity electrical stimulation to prevent the loss of muscle mass, strength, and endurance in spaceflight and in patients with severe chronic diseases. This study investigated the effects of a one-week disuse, both with and without low-intensity neuromuscular electrical stimulation – a safe (non-traumatic) approach to prevent the loss of muscle mass, on the functional capacities and gene expression in thigh and calf muscles. This study assessed the efficiency of low-intensity (~10% of maximal voluntary contraction) electrical stimulation in preventing the negative effects of 7-day disuse (dry immersion without [see a related dataset GSE271607] and with daily stimulation) on the strength and aerobic performance of the ankle plantar flexors and knee extensors, mitochondrial function in permeabilized muscle fibers, and the proteomic (quantitative mass spectrometry-based analysis) and transcriptomic (RNA-sequencing) profiles of the soleus muscle and vastus lateralis muscle. Application of electrical stimulation during dry immersion prevented a decrease in the maximal strength and a slight reduction in aerobic performance of the knee extensors, as well as a decrease in maximal (intrinsic) ADP-stimulated mitochondrial respiration and changes in the expression of genes encoding mitochondrial, extracellular matrix, and membrane proteins in the vastus lateralis muscle. In contrast, for the ankle plantar flexors/soleus muscle, electrical stimulation had a positive effect only on maximal mitochondrial respiration, but slightly accelerated the decline in the maximal strength and muscle fiber cross-sectional area, which appears to be related to the activation of inflammatory genes. The data obtained open up broad prospects for the use of low-intensity electrical stimulation to prevent the negative effects of disuse for “mixed” muscles, meanwhile, the optimization of the stimulation protocol is required for “slow” muscles.
2024-09-08 | GSE271606 | GEO
Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
2024-12-31 | E-MTAB-14061 | biostudies-arrayexpress
Project description:Microbiome research related to muscle strength improvement
| PRJEB85118 | ENA