Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA90079 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and decreased regenerative capacity, which can lead to sarcopenia and increased mortality. While the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Therefore, identification of signaling pathways affecting satellite cell function during aging may provide insights into therapeutic targets for combating sarcopenia. Here, we show that a cell-autonomous loss in self-renewal occurs via novel alterations in FGF and p38αβ MAPK signaling in old satellite cells. We further demonstrate that pharmacological manipulation of these pathways can ameliorate age-associated self-renewal defects. Thus, our data highlight an age-associated deregulation of a satellite cell homeostatic network and reveals potential therapeutic opportunities for the treatment of progressive muscle wasting. Satellite cells were isolated from young (3-6mo) and aged (20-25mo) adult mice; individual date files represent 2 independent pools of RNA from 4-8 mice at each timepoint.
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Project description:Sarcopenia, characterized by the loss of muscle mass, strength, and function, predisposes adverse outcomes and its mechanism is waiting to reveal. Here, we report decrease of PRR14, a nuclear protein, in skeletal muscle results in sarcopenia. Genetically, genome-wide association studies (GWAS) identified multiple single nucleotide polymorphisms (SNPs) in PRR14 locus associated with body mass index (BMI) and total body lean mass, which indicated its association with sarcopenia; Specific knockout of skeletal muscle Prr14 in mice confirmed the causal effect; Biochemical analysis and high-throughput sequencing, including both transcriptome and approaches for the study of the epigenome (CUT&Tag sequencing and ATAC sequencing), revealed that Prr14 was required for myofiber homeostasis in skeletal muscle: Prr14 loss altered chromatin structure and reduced Mef2c activity, which in combination resulted in failure of maintaining myofiber identity and therefore sarcopenia. Our findings demonstrate that PRR14 orchestrates critical epigenetic changes and transcription factor activity to maintain myofiber identity, thereby providing novel therapeutic avenues for skeletal muscle pathologies associated with dysregulation of these mechanisms.
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Project description:Aging associates with progressive loss of skeletal muscle function leading up to sarcopenia, a process characterized by impaired mobility and weakening of muscle strength. Molecular mechanisms underpinning sarcopenia are still poorly characterized. Since aging associates with profound epigenetic changes, epigenetic landscape alteration analysis in the skeletal muscle promises to highlight molecular mechanisms of age-associated sarcopenia. The study was conducted exploiting the short-lived Nothobranchius furzeri (Nfu), a relatively new model for aging studies. The epigenetic analysis suggested for a less accessible and more condensed chromatin structure in old Nfu skeletal muscle. Specifically, an accumulation of heterochromatin regions was observed as consequence of increased levels of H3K27me3, HP1a, polycomb complex subunits and senescence associated heterochromatic foci (SAHFs). Consistently, euchromatin histone marks, including H3K9ac, decreased. The integrative bioinformatics analysis of RNASeq and ChIPSeq, related to skeletal muscle of Nfu at different ages, revealed a down-modulation of transcripts involved in cell cycle, differentiation and DNA repair and an up-regulation of inflammation and senescence genes. Undoubtedly, more studies are needed to disclose the detailed mechanisms, but this approach shed light on unprecedented specific features of Nfu skeletal muscle aging, potentially associated with sarcopenia onset and consequent impairment of swimming and mobility typical of old Nfu.
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Project description:Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and decreased regenerative capacity, which can lead to sarcopenia and increased mortality. While the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Therefore, identification of signaling pathways affecting satellite cell function during aging may provide insights into therapeutic targets for combating sarcopenia. Here, we show that a cell-autonomous loss in self-renewal occurs via novel alterations in FGF and p38αβ MAPK signaling in old satellite cells. We further demonstrate that pharmacological manipulation of these pathways can ameliorate age-associated self-renewal defects. Thus, our data highlight an age-associated deregulation of a satellite cell homeostatic network and reveals potential therapeutic opportunities for the treatment of progressive muscle wasting.
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Project description:Age-related sarcopenia is associated with a variety of changes in skeletal muscle. These changes are interrelated with each other and associated with systemic metabolism, the details of which, however, are largely unknown. Eicosapentaenoic acid (EPA) is a promising nutrient against sarcopenia and has multifaceted effects on systemic metabolism. Although several human studies have suggested that EPA supplementation protects against sarcopenia, the causal relationship of EPA supplementation and an increase of muscle strength has poor evidence in vivo. We demonstrated that aging skeletal muscle in male mice shows lower grip strength and fiber type changes, both of which can be inhibited by EPA supplementation irrespective of muscle mass alteration. We hypothesized that the aging process in skeletal muscle can be intervened by the administration of EPA, via transcriptomic changes in skeletal muscle. This analysis revealed fast-to-slow fiber type transition in aging muscle, which was partially inhibited by EPA.
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Project description:the expression of TF MEF2C is decreased in skeletal muscle of PRR14-KO mice,which displays sarcopenia phenotype. Meanwhile, increasing MEF2C's expression in skeletal muscle lessens the phenotype.
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Project description:Sarcopenia, characterized by the loss of muscle mass, strength, and function, predisposes adverse outcomes and its mechanism is waiting to reveal. Here, we report decrease of PRR14, a nuclear protein, in skeletal muscle results in sarcopenia. Genetically, genome-wide association studies (GWAS) identified multiple single nucleotide polymorphisms (SNPs) in PRR14 locus associated with body mass index (BMI) and total body lean mass, which indicated its association with sarcopenia; Specific knockout of skeletal muscle Prr14 in mice confirmed the causal effect; Biochemical analysis and high-throughput sequencing, including both transcriptome and approaches for the study of the epigenome (CUT&Tag sequencing and ATAC sequencing), revealed that Prr14 was required for myofiber homeostasis in skeletal muscle: Prr14 loss altered chromatin structure and reduced Mef2c activity, which in combination resulted in failure of maintaining myofiber identity and therefore sarcopenia. Our findings demonstrate that PRR14 orchestrates critical epigenetic changes and transcription factor activity to maintain myofiber identity, thereby providing novel therapeutic avenues for skeletal muscle pathologies associated with dysregulation of these mechanisms.
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