Comparison of age-related changes in gene expression of 2 rat skeletal muscles
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA612538 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:As a result of aging, skeletal muscle undergoes atrophy and a decrease in function. This age-related skeletal muscle weakness is known as “sarcopenia.” To understand the changes in gene expression that occur as a result of age in skeletal muscles, we generated a multi-time point gene expression signature throughout the lifespan of mice and rats, as these are the most commonly used species in preclinical research and intervention testing
2023-06-19 | GSE226118 | GEO
Project description:Comparison of age-related changes in gene expression of 2 rat skeletal muscles (20 months, 22 months)
| PRJNA612539 | ENA
Project description:As a result of aging, skeletal muscle undergoes atrophy and a decrease in function. This age-related skeletal muscle weakness is known as “sarcopenia.” To understand the changes in gene expression that occur as a result of age in skeletal muscles, we generated a multi-time point gene expression signature throughout the lifespan of mice and rats, as these are the most commonly used species in preclinical research and intervention testing
2023-06-19 | GSE226117 | GEO
Project description:In this study we compared Gastrocnemius and Triceps gene expression with age. Our results show that gene expression is massively modulated with age in Gastroc but on the contrary very stable in Triceps, suggesting that Triceps is resistant to age-related defects. 3 groups of age (8 months, 18 months and 24 months) were analyzed, with 9-10 replicates per group. Gastrocnemius and Triceps were collected for each animal.
2016-05-12 | E-GEOD-78702 | biostudies-arrayexpress
Project description:In this study we compared Gastrocnemius and Triceps gene expression with age. Our results show that gene expression is massively modulated with age in Gastroc but on the contrary very stable in Triceps, suggesting that Triceps is resistant to age-related defects.
2020-03-14 | GSE146976 | GEO
Project description:Skeletal muscle atrophy is one of the critical issues which elderly people face. The precise mechanism underlying muscle atrophy during aging is not fully understood. In order to identify miRNA whose expression is changed in age-associated muscle atrophy, we performed miRNA expression profiling of skeletal muscles in young and aged rats. Microarray analysis revealed differential miRNA expression in EDL and soleus muscles of aged rats compared with those of young rats. We next investigated whether the age-associated changes of miRNA expression observed in rats were recapitulated in mice and found that the expression level of miR-206 in EDL muscle and that of miR-196a in EDL and soleus muscles were respectively higher and lower in aged rodents than in young rodents. In mouse C2C12 myoblasts and myotubes, introduction of miR-196a decreased the protein level of Forkhead-box transcription factor Foxo1, a known target of miR-196a, indicating that miR-196a may regulate Foxo1 expression also in skeletal muscles. Furthermore, miR-196a overexpression exacerbated cell death caused by an exposure to hydrogen peroxide. Lastly, we demonstrated that expression of Foxo1 was elevated in EDL and soleus muscles of aged mice compared with those of young mice. These results suggest that miRNAs are involved in skeletal muscle atrophy during aging and that decreased miR-196a expression may protect skeletal muscle cells from oxidative stress in part through induction of Foxo1.
2016-08-31 | GSE70990 | GEO
Project description:The right legs of 8 Brown-Norway male rats were denervated by a high sciatic nerve section in the hip region of the hind limb.Two months after denervation (6 months of age), extensor digitorum longus (EDL) muscles were removed from the operated legs. The EDL muscles from 8 age-matched non-operated rats served as innervated controls. Total RNA was isolated, labeled cDNA was prepared and hybridized to the Rat Atlas 1.2 Array II membranes (Clontech Laboratories, Palo Alto, CA). Keywords: other
2004-09-10 | GSE1741 | GEO
Project description:In this study we compared Gastrocnemius and Triceps gene expression with age. Our results show that gene expression is massively modulated with age in Gastroc but on the contrary very stable in Triceps, suggesting that Triceps is resistant to age-related defects.
2016-05-12 | GSE78702 | GEO
Project description:During aging, the number and functionality of muscle stem cells (MuSCs) decreases leading to impaired regeneration of aged skeletal muscle. In addition to intrinsic changes in aged MuSCs, extracellular matrix (ECM) proteins deriving from other cell types, e.g., fibrogenic-adipogenic progenitor cells (FAPs), contribute to the aging phenotype of MuSCs and impaired regeneration in the elderly. So far, no comprehensive analysis on how age-dependent changes in the whole skeletal muscle proteome affect MuSC function have been conducted. Here, we investigated age-dependent changes in the proteome of different skeletal muscle types by applying deep quantitative mass spectrometry. We identified 183 extracellular matrix proteins that show different abundances in skeletal muscles of old mice. By integrating single cell sequencing data, we reveal that transcripts of those ECM proteins are mainly expressed in FAPs, suggesting that FAPs are the main contributors to ECM remodelling during aging. We functionally investigated one of those ECM molecules, namely Smoc2, which is aberrantly expressed during aging. We show that Smoc2 levels are elevated during regeneration and that its accumulation in the aged MuSC niche causes impairment of MuSCs function through constant activation of integrin/MAPK signaling. In vivo, supplementation of exogenous Smoc2 hampers the regeneration of young muscles following serial injuries, leading to a phenotype reminiscent of regenerating aged skeletal muscle. Taken together, we provide a comprehensive resource of changes in the composition of the ECM of aged skeletal muscles, we pinpoint the cell types driving these changes, and we identify a new niche protein causing functional impairment of MuSCs thereby hampering the regeneration capacity of skeletal muscles.
2021-11-25 | PXD015616 | Pride
Project description:During aging, the number and functionality of muscle stem cells (MuSCs) decreases leading to impaired regeneration of aged skeletal muscle. In addition to intrinsic changes in aged MuSCs, extracellular matrix (ECM) proteins deriving from other cell types, e.g., fibrogenic-adipogenic progenitor cells (FAPs), contribute to the aging phenotype of MuSCs and impaired regeneration in the elderly. So far, no comprehensive analysis on how age-dependent changes in the whole skeletal muscle proteome affect MuSC function have been conducted. Here, we investigated age-dependent changes in the proteome of different skeletal muscle types by applying deep quantitative mass spectrometry. We identified 183 extracellular matrix proteins that show different abundances in skeletal muscles of old mice. By integrating single cell sequencing data, we reveal that transcripts of those ECM proteins are mainly expressed in FAPs, suggesting that FAPs are the main contributors to ECM remodelling during aging. We functionally investigated one of those ECM molecules, namely Smoc2, which is aberrantly expressed during aging. We show that Smoc2 levels are elevated during regeneration and that its accumulation in the aged MuSC niche causes impairment of MuSCs function through constant activation of integrin/MAPK signaling. In vivo, supplementation of exogenous Smoc2 hampers the regeneration of young muscles following serial injuries, leading to a phenotype reminiscent of regenerating aged skeletal muscle. Taken together, we provide a comprehensive resource of changes in the composition of the ECM of aged skeletal muscles, we pinpoint the cell types driving these changes, and we identify a new niche protein causing functional impairment of MuSCs thereby hampering the regeneration capacity of skeletal muscles.
2021-11-25 | PXD015728 | Pride