Effects of Denervation on Muscle Function
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1065865 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27598300.fastq.gz | Fastqsanger.gz | |||
| SRR27598301.fastq.gz | Fastqsanger.gz | |||
| SRR27598302.fastq.gz | Fastqsanger.gz | |||
| SRR27598291.fastq.gz | Fastqsanger.gz | |||
| SRR27598292.fastq.gz | Fastqsanger.gz |
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Project description:Muscle denervation causes skeletal muscle atrophy. The goal of these studies was to determine the effects of denervation on skeletal muscle mRNA levels in C57BL/6 mice. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012.
2012-09-15 | GSE39195 | GEO
Project description:Genistein is one of the flabonoids which is included in high concentration in soy and has a high estrogenic activity. Beneficial effects of estrogen or hormone replacement therapy (HRT) on muscle mass or muscle atrophy have been demonstrated. We investigated the preventive effects and underlying mechanisms of genistein intake on denervation-induced muscle atrophy. Genistein intake significantly suppressed the loss of soleus muscle weight and the denervation-induced up-regulations of FOXO1 protein. The results of a DNA microarray showed that the estrogen receptor (ER) target genes are changed by genistein intake. Genistein suppressed the soleus muscle atrophy, and it was attenuated under the ER antagonist treatment. The administration of an ERα agonist suppressed the denervation-induced muscle atrophy and up-regulation of Atrogin1 gene expression, but the ERβ agonist had no effect.
2016-01-23 | GSE77121 | GEO
Project description:Muscle denervation causes skeletal muscle atrophy. The goal of these studies was to determine the effects of denervation on skeletal muscle mRNA levels in C57BL/6 mice. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Left sciatic nerves of C57BL/6 mice were transected. Seven days later bilateral tibialis anterior muscles were harvested. mRNA levels in denervated muscles were normalized to levels in contralateral innervated muscles.
2012-09-15 | E-GEOD-39195 | biostudies-arrayexpress
Project description:The functional state of denervated muscle is a critical factor in the ability to restore movement after injury- or disease-related paralysis. Here we used peripheral optogenetic stimulation in the mouse whisker system to investigate the time course of changes in nerve and muscle function following facial nerve transection. While most skeletal muscles atrophy after lower motor neuron denervation, optogenetic muscle stimulation of the paralyzed whisker pad revealed sustained increases in the sensitivity, velocity, and amplitude of whisker movements, and reduced fatigability, starting 48 h after denervation. Transcriptome profiling showed distinct regulation of multiple gene families in denervated whisker pad muscles compared to the atrophy-prone soleus, including prominent changes in ion channels and contractile fibers. Together, our results define the functional and transcriptomic landscape of muscle denervation supersensensitivty, and have implications for restoring movement after neuromuscular injury or disease.
2018-11-19 | GSE121590 | GEO
Project description:Innervation of skeletal muscle fibers plays a crucial role in the maintenance of muscle tone and normal functioning, but little is known to date about denervated muscle atrophy and its underlying mechanisms. To this end, we performed RNA sequencing of skeletal muscle from sciatic nerve-excised C57BL/6 and BALB/c mice to investigate the underlying mechanisms of denervated skeletal muscle atrophy.
2024-10-31 | GSE253469 | GEO
Project description:Background: Skeletal muscle function crucially depends on motor innervation and after injury on the resident muscle stem cells (MuSCs). However, it is poorly understood how innervation affects MuSC properties. Methods: We investigated the alterations of MuSCs and their immediate niche, the myofiber, after denervation in a surgery-based mouse model of unilateral sciatic nerve transection. FACS-isolated MuSCs were subjected to transcriptomics and proteomics analyses to investigate which changes occur after denervation. We performed Cardiotoxin-induced muscle injury, MuSC transplantation and floating myofiber cultures to assess MuSC functionality after denervation in addition to bioinformatics and histological analyses. Results: We observed a significant increase in the number of MuSCs (Pax7 positive; p-value= 0.0441), proliferating MuSCs (Pax7/Ki67 positive; p-value= 0.0023), activated MuSCs (MyoD positive; p-value= 0.0016) and differentiating MuSCs (Myog positive; p-value= 0.0057) after denervation. This aberrant activation and premature commitment of MuSCs to the myogenic lineage was accompanied by profound alterations on the mRNA (2613 differentially expressed genes, adj. p-value <0.05) and protein (1096 differentially abundant proteins, q-value <0.05) level after denervation. MuSCs from denervated hosts still engrafted and fused to form new myofibers irrespective of the innervation status of the recipient, suggesting the MuSC niche is driving alterations in MuSCs after denervation. The myofiber transcriptome after denervation showed massive changes in the general expression profile (10492 DEGs, p-value <0.05) and in several predicted secreted factors. Incubation of myofiber-associated MuSCs with supernatant from denervated myofibers increased cluster formation, reinforcing myofibers as a source of secreted factors driving MuSC alterations after denervation. Opn and Tgfb1 showed an increased secretion by denervated myofibers (30-fold and 6000-fold, respectively), and incubation with Tgfb1 alone induced Junb expression in myogenic cells, one of the genes highly upregulated in MuSCs after denervation (p-value= 1.85e-18, log2fc= 3.27), demonstrating that myofiber-secreted ligands influence MuSC gene expression. A combination of skeletal muscle injury and denervation led to reduced numbers of proliferating MuSCs (Sham: 47 vs DEN: 19.75 cells per cross section 10 days post-injury) and sustained high levels of developmental myosin heavy chain (Sham: 1 % vs DEN: 40 % of all myofibers 21 days post-injury), indicating hampered MuSC functionality due to changes in the microenvironment. Conclusion: Denervation of skeletal muscle causes alterations in myofiber secretion, leading to activation and profound changes of MuSCs, ultimately resulting in a reduced regenerative capacity. As these alterations are partially reversible, MuSCs are a promising target for novel treatment options for neuromuscular disorders and peripheral nerve injuries.
2024-03-04 | GSE217928 | GEO
Project description:Background: Skeletal muscle function crucially depends on motor innervation and after injury on the resident muscle stem cells (MuSCs). However, it is poorly understood how innervation affects MuSC properties. Methods: We investigated the alterations of MuSCs and their immediate niche, the myofiber, after denervation in a surgery-based mouse model of unilateral sciatic nerve transection. FACS-isolated MuSCs were subjected to transcriptomics and proteomics analyses to investigate which changes occur after denervation. We performed Cardiotoxin-induced muscle injury, MuSC transplantation and floating myofiber cultures to assess MuSC functionality after denervation in addition to bioinformatics and histological analyses. Results: We observed a significant increase in the number of MuSCs (Pax7 positive; p-value= 0.0441), proliferating MuSCs (Pax7/Ki67 positive; p-value= 0.0023), activated MuSCs (MyoD positive; p-value= 0.0016) and differentiating MuSCs (Myog positive; p-value= 0.0057) after denervation. This aberrant activation and premature commitment of MuSCs to the myogenic lineage was accompanied by profound alterations on the mRNA (2613 differentially expressed genes, adj. p-value <0.05) and protein (1096 differentially abundant proteins, q-value <0.05) level after denervation. MuSCs from denervated hosts still engrafted and fused to form new myofibers irrespective of the innervation status of the recipient, suggesting the MuSC niche is driving alterations in MuSCs after denervation. The myofiber transcriptome after denervation showed massive changes in the general expression profile (10492 DEGs, p-value <0.05) and in several predicted secreted factors. Incubation of myofiber-associated MuSCs with supernatant from denervated myofibers increased cluster formation, reinforcing myofibers as a source of secreted factors driving MuSC alterations after denervation. Opn and Tgfb1 showed an increased secretion by denervated myofibers (30-fold and 6000-fold, respectively), and incubation with Tgfb1 alone induced Junb expression in myogenic cells, one of the genes highly upregulated in MuSCs after denervation (p-value= 1.85e-18, log2fc= 3.27), demonstrating that myofiber-secreted ligands influence MuSC gene expression. A combination of skeletal muscle injury and denervation led to reduced numbers of proliferating MuSCs (Sham: 47 vs DEN: 19.75 cells per cross section 10 days post-injury) and sustained high levels of developmental myosin heavy chain (Sham: 1 % vs DEN: 40 % of all myofibers 21 days post-injury), indicating hampered MuSC functionality due to changes in the microenvironment. Conclusion: Denervation of skeletal muscle causes alterations in myofiber secretion, leading to activation and profound changes of MuSCs, ultimately resulting in a reduced regenerative capacity. As these alterations are partially reversible, MuSCs are a promising target for novel treatment options for neuromuscular disorders and peripheral nerve injuries.
2024-03-04 | GSE217929 | GEO
Project description:Muscle atrophy is associated with aging (sarcopenia) and chronic unloading (such as bed confinement and immobilization with casts), as well as various pathological conditions such as type 1 diabetes and nerve injury (denervation). C57BL/6 mice (7 weeks old, male) were denervated. After 14 days, skeletal muscle was collected and RNA extracted. Expression of Dnmt3a was reduced while expression of Gdf5 was increased by denervation.
2019-04-01 | GSE97313 | GEO
Project description:Analysis of denervation induced regulation of muscle mass at gene expression level. The hypothesis tested in the present study was that the presence of MuRF1 contributes to the extent of gene expression changes observed in specific sets of genes during a challenge leading to muscle atrophy. Results provide important information on the response of triceps surae muscle to sciatic nerve resection (denervation), such as specific structural, metabolic, and neuromuscular junction associated genes, that may be influenced by MuRF1 during atrophy. Total RNA obtained from isolated triceps surae muscle subjected to 3 or 14 days post-denervation compared to nonsurgically treated littermate control muscles.
2013-02-12 | E-GEOD-44205 | biostudies-arrayexpress
Project description:To assess the m6A methylome during denervation-induced muscle atrophy, the methylated RNA immunoprecipitation sequencing (MeRIP-seq) was performed.
2021-09-26 | GSE179178 | GEO