Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1217610 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Aged (22-mo) female mice (n=35), obtained from the US NIH National Institute on Aging (NIA) Aged Rodent Colony, were randomly assigned to one of four groups: saline-treated sedentary ( n=9), nicotinamide N-methyltransferase inhibitor (NNMTi)-treated sedentary (10 mg/kg body weight; n=9), saline-treated progressive weighted wheel running (PoWeR; saline; n=10), and NNMTi-treated PoWeR (10 mg/kg body weight; n=7) . Group-housed Sed cohorts were compared to singly-housed PoWeR cohorts that underwent a 1-week introduction to an unweighted wheel, followed by eight weeks of weighted wheel running. Forelimb grip strength was assessed by a single NNMTi treatment-blinded investigator during week six and averaged across 2-4 trials/mouse. At the end of week 8, when mice were ~24.5-months-old, the strength of the right limb plantarflexor muscle complex was measured using an in vivo isometric peak tetanic torque technique and a fatigue test. After the fatigue test, mice were euthanized, and tissues were weighed and collected. Of note, hindlimb muscles from the right limb (the limb that underwent in vivo isometric peak tetanic torque and fatigue testing) were processed for immunohistochemistry to avoid acute effects of muscle functional testing on the proteome and metabolome. Hindlimb muscles from the left limb that did not undergo torque and fatigue testing were flash-frozen for proteome and metabolome analyses.
2024-05-07 | MSV000094700 | MassIVE
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:Parkinson's disease (PD) is defined by neurodegeneration, muscle atrophy, and bone deterioration, largely due to dopamine depletion. This study evaluates the therapeutic potential of heat-killed Enterococcus faecium FBL1 (HEF) in mitigating PD-related dysfunction through osteoblastogenesis and neurogenesis pathways. In the rotarod test, MPTP-treated mice exhibited a significant reduction in walking time, 4.1 times lower than that of the normal group. However, treatment with HDF notably improved the retention time, with a dose-dependent increase, compared to MPTP group. Wire-hanging test showed enhanced muscle strength, as HEF-treated mice demonstrated a 2.1- and 3.3-fold increase in the latency to fall at low and high doses, respectively, when compared to MPTP group. Grip strength and forced swim test, further supported the findings of neuromuscular recovery and reduced immobility in the HEF treated mice. The alpha-synuclein aggregation in the brain and muscle induced by MPTP were attenuated by HEF. Volcano plot analysis of muscle tissue revealed that MPTP treatment caused significant dysregulation, with 142 upregulated and 163 downregulated genes, including the downregulation of Wnt signaling-related genes Astn1 and Frat2, which are involved in neurogenesis and muscle regeneration. Conversely, the osteogenesis-related gene Pbx1 was upregulated by HEF, compared to MPTP treated group. Treatment with HEF also restored gene expression, notably increasing Tnxb, essential for tissue integrity, and Gsn, involved in various biological processes, compared with MPTP. Key markers of skeletal muscle differentiation (Myf5, MyoG, Myh1), osteoblastogenesis (Bmp2, Bmp4, SMAD1/5/8, RUNX2), and neurogenesis (Wnt3a, Beta-catenin, TCF1, LEF1) were downregulated in MPTP-induced PD but restored by HEF. Inflammatory markers (TNF-alpha, iNOS, and NF-kappaB) were significantly elevated in the MPTP group. However, these levels were reduced by HEF in a dose-dependently. This study highlights the pivotal role of osteoblastogenic (BMP/SMAD signaling) and neurogenic (Wnt signaling) pathways in maintaining muscle and bone homeostasis in PD. HEF offers a novel therapeutic approach targeting the BMP/SMAD and Wnt signaling pathways to mitigate muscle and bone degeneration in patients with PD.
2024-12-22 | GSE284676 | GEO
Project description:To test the hypothesis that different muscles may express variable amounts of different isoforms of muscle genes, we applied a custom-designed exon microarray containing probes for 57 muscle-specific genes to assay the transcriptional profiles in sets of human adult, lower limb skeletal muscles.
2015-06-17 | GSE69938 | 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