Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA262975 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Fast and slow skeletal muscles show different characteristics and phenotypes. This data obtained from microarray includes the comparison of normal fast plantaris and slow soleus muscles of adult rats. Characters of slow muscle are strongly dependent on the level of muscular activity. Denervation silences the muscular activity. Therefore, we determined the effects of denervation on gene expression in slow soleus muscle of adult rats.
2014-10-04 | GSE62028 | GEO
Project description:Skeletal muscle denervation is a characteristic feature of neuromuscular diseases such as amyotrophic lateral sclerosis (ALS) and sarcopenia, leading to atrophy, loss of muscle strength, and poor patient outcomes. Myofibers are typically classified into slow oxidative and fast glycolytic types based on their contractile and metabolic properties. Neuromuscular diseases predominantly affect fast myofibers, while slow myofibers are relatively spared. However, the mechanisms underlying the heightened susceptibility of fast myofibers to disease and atrophy remain unclear. To investigate this, we analyzed the transcriptional profiles of innervated and denervated myonuclei. Our findings revealed that the fast muscle gene program and the transcription factor Maf are repressed during denervation. Notably, overexpression of Maf in the skeletal muscles of mice prevented loss of muscle mass and myofiber atrophy caused by denervation. Single-nucleus RNA sequencing and ATAC sequencing demonstrated that Maf overexpression reprogrammed denervated myonuclei by repressing atrophic gene programs and reactivating fast muscle gene expression. Similar repression of fast muscle genes and Maf was observed in muscles from mice and humans with ALS. Consistent with these findings, Maf overexpression in human skeletal muscle cells induced the expression of fast muscle genes while suppressing atrophic gene expression. Our findings highlight a key role for Maf in maintaining muscle mass and demonstrate that its repression contributes to the progression of neuromuscular diseases in both mice and humans. Modulating Maf activity could offer a promising therapeutic strategy to preserve skeletal muscle function during disease, aging, or injury.
2025-05-29 | GSE298187 | GEO
Project description:Skeletal muscle denervation is a characteristic feature of neuromuscular diseases such as amyotrophic lateral sclerosis (ALS) and sarcopenia, leading to atrophy, loss of muscle strength, and poor patient outcomes. Myofibers are typically classified into slow oxidative and fast glycolytic types based on their contractile and metabolic properties. Neuromuscular diseases predominantly affect fast myofibers, while slow myofibers are relatively spared. However, the mechanisms underlying the heightened susceptibility of fast myofibers to disease and atrophy remain unclear. To investigate this, we analyzed the transcriptional profiles of innervated and denervated myonuclei. Our findings revealed that the fast muscle gene program and the transcription factor Maf are repressed during denervation. Notably, overexpression of Maf in the skeletal muscles of mice prevented loss of muscle mass and myofiber atrophy caused by denervation. Single-nucleus RNA sequencing and ATAC sequencing demonstrated that Maf overexpression reprogrammed denervated myonuclei by repressing atrophic gene programs and reactivating fast muscle gene expression. Similar repression of fast muscle genes and Maf was observed in muscles from mice and humans with ALS. Consistent with these findings, Maf overexpression in human skeletal muscle cells induced the expression of fast muscle genes while suppressing atrophic gene expression. Our findings highlight a key role for Maf in maintaining muscle mass and demonstrate that its repression contributes to the progression of neuromuscular diseases in both mice and humans. Modulating Maf activity could offer a promising therapeutic strategy to preserve skeletal muscle function during disease, aging, or injury.
2025-05-29 | GSE298184 | GEO
Project description:We performed the first quantitative proteomics analysis of differences between striated (fast) and catch (slow) adductor muscle in Yesso scallop (Patinopecten yessoensis), with the goal to uncover muscle specific genes and proteins, as well as enzymes of metabolic pathways in fast and slow adductor muscle of scallops. The present findings highlight the functional roles of muscle contractile proteins, calcium signaling pathways, membrane and extracellular matrix proteins, and glycogen metabolism involved in the different contractile and metabolic properties between fast and slow muscles. The present findings will help better understand the molecular basis underlying muscle contraction and its physiological regulation in invertebrates.
2018-10-26 | PXD005166 | Pride
Project description:Fast and slow skeletal muscles show different characteristics and phenotypes. This data obtained from microarray includes the comparison of normal fast plantaris and slow soleus muscles of adult rats. Characters of slow muscle are strongly dependent on the level of muscular activity. Denervation silences the muscular activity. Therefore, we determined the effects of denervation on gene expression in slow soleus muscle of adult rats. Denervation was performed by transection (~5 mm) of left sciatic nerve at the gluteal level. No treatments were made in the normal control rats. Sampling of soleus and/or plantaris was performed in both normal and experimental groups 28 days after the surgery.
2014-10-04 | E-GEOD-62028 | biostudies-arrayexpress
Project description:Innervated and 2 month Denervated Rat EDL muscles
| PRJNA90361 | ENA
Project description:Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease that progressively debilitates neuronal cells that control voluntary muscle activity. In a mouse model of ALS that expresses mutated human superoxide dismutase 1 (SOD1-G93A) skeletal muscle is one of the tissues affected early by mutant SOD1 toxicity. Fast-twitch and slow-twitch muscles are differentially affected in ALS patients and in the SOD1-G93A model, fast-twitch muscles being more vulnerable. We used miRNA microarrays to investigate miRNA alterations in fast-twitch (EDL) and slow-twitch (soleus) skeletal muscles of symptomatic SOD1-G93A animals and their age-matched wild type littermates.
2014-03-04 | GSE55507 | GEO
Project description:Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease that progressively debilitates neuronal cells that control voluntary muscle activity. In a mouse model of ALS that expresses mutated human superoxide dismutase 1 (SOD1-G93A) skeletal muscle is one of the tissues affected early by mutant SOD1 toxicity. Fast-twitch and slow-twitch muscles are differentially affected in ALS patients and in the SOD1-G93A model, fast-twitch muscles being more vulnerable. We used miRNA microarrays to investigate miRNA alterations in fast-twitch (EDL) and slow-twitch (soleus) skeletal muscles of symptomatic SOD1-G93A animals and their age-matched wild type littermates. At age of 90 days RNA was extracted from extensor digitorum longus (EDL) and soleus (SOL) muscles of male SOD1-G93A animals and their age-matched wild type male littermates. RNA was hybridized on Affymetrix Multispecies miRNA-2_0 Array.
2014-03-04 | E-GEOD-55507 | biostudies-arrayexpress
Project description:We used phosphoproteomic profiling of slow-twitch (soleus, SOL) and fast-twitch (biceps femoris, BF) muscle to identify differences between these muscle types.
2022-08-16 | PXD036066 |
Project description:Muscle is highly hierarchically organized, with functions shaped by genetically controlled expression of protein ensembles with different isoform profiles at the sarcomere scale. However, it remains unclear how isoform profiles shape whole-muscle performance. We compared two mouse hindlimb muscles, the slow, relatively parallel-fibered soleus and the faster, more pennate-fibered tibialis anterior (TA), across scales: from gene regulation, isoform expression and translation speed, to force-length-velocity-power for intact muscles. Expression of myosin heavy-chain (MHC) isoforms directly corresponded with contraction velocity. The fast-twitch TA with fast MHC isoforms had faster unloaded velocities (actin sliding velocity, Vactin; peak fiber velocity, Vmax) than the slow-twitch soleus. For the soleus, Vactin was biased towards Vactin for purely slow MHC I, despite this muscle's even fast and slow MHC isoform composition. Our multi-scale results clearly identified a consistent and significant dampening in fiber shortening velocities for both muscles, underscoring an indirect correlation between Vactin and fiber Vmax that may be influenced by differences in fiber architecture, along with internal loading due to both passive and active effects. These influences correlate with the increased peak force and power in the slightly more pennate TA, leading to a broader length range of near-optimal force production. Conversely, a greater force-velocity curvature in the near-parallel fibered soleus highlights the fine-tuning by molecular-scale influences including myosin heavy and light chain expression along with whole-muscle characteristics. Our results demonstrate that the individual gene, protein and whole-fiber characteristics do not directly reflect overall muscle performance but that intricate fine-tuning across scales shapes specialized muscle function.
2022-05-23 | GSE203400 | GEO