Rattus norvegicus
Ontology highlight
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:We used phosphoproteomic profiling of slow-twitch (soleus, SOL) and fast-twitch (biceps femoris, BF) muscle to identify differences between these muscle types.
| PXD036066 |
Project description:Here, we characterize the genomic landscape of four mouse hindlimb muscles that differ in slow myofiber content at two time points (E18.5 and adult) to identify novel enhancers that may underlie the expression of genes involved in myofiber development and physiology. RNA-seq analysis revealed that fast- and slow-biased muscles show divergent patterns of gene regulation beginning at a late embryonic time point and persisting through adulthood. Genes differentially expressed between adult fast- and slow-biased muscles were enriched with biological pathways unique to each myofiber type, with glycolytic pathways characterizing adult fast-biased muscles and mitochondrial biogenesis and lipid metabolism characterizing adult slow-biased muscles. By integrating differential expression analysis (RNA-seq) with differential accessibility analysis (ATAC-seq) we identified twelve conserved, muscle-specific candidate enhancers nearby differentially expressed genes that regulate cell metabolism and the genetic markers of myofiber type. Nine candidate enhancers significantly increased and three significantly decreased luciferase reporter activities in C2C12 cells, highlighting the dynamic role of tissue-specific enhancers and repressors on development and differentiation. However, further validation is needed to see if these enhancers regulate the expression of target genes and the effect on muscle myofiber content. Collectively, these results highlight the importance of conserved, skeletal muscle-specific enhancers on skeletal muscle development and adult myofiber phenotypes and provide additional genomic targets for further validation.
2026-02-24 | GSE292230 | GEO
Project description:Here, we characterize the genomic landscape of four mouse hindlimb muscles that differ in slow myofiber content at two time points (E18.5 and adult) to identify novel enhancers that may underlie the expression of genes involved in myofiber development and physiology. RNA-seq analysis revealed that fast- and slow-biased muscles show divergent patterns of gene regulation beginning at a late embryonic time point and persisting through adulthood. Genes differentially expressed between adult fast- and slow-biased muscles were enriched with biological pathways unique to each myofiber type, with glycolytic pathways characterizing adult fast-biased muscles and mitochondrial biogenesis and lipid metabolism characterizing adult slow-biased muscles. By integrating differential expression analysis (RNA-seq) with differential accessibility analysis (ATAC-seq) we identified twelve conserved, muscle-specific candidate enhancers nearby differentially expressed genes that regulate cell metabolism and the genetic markers of myofiber type. Nine candidate enhancers significantly increased and three significantly decreased luciferase reporter activities in C2C12 cells, highlighting the dynamic role of tissue-specific enhancers and repressors on development and differentiation. However, further validation is needed to see if these enhancers regulate the expression of target genes and the effect on muscle myofiber content. Collectively, these results highlight the importance of conserved, skeletal muscle-specific enhancers on skeletal muscle development and adult myofiber phenotypes and provide additional genomic targets for further validation.
2026-02-24 | GSE292232 | GEO