Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA344669 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Epigenetic stress responses induce muscle stem cell aging by Hoxa9 developmental signals
| PRJNA347647 | ENA
Project description:Epigenetic stress responses induce muscle stem cell aging by Hoxa9 developmental signals [microarray]
| PRJNA347652 | ENA
Project description:Epigenetic determinants of muscle stem cell quiescence and chronological aging
| PRJNA205033 | ENA
Project description:To uncover new pathways that are important for skeletal muscle stem cell aging, we performed multiomics profiling, including transcriptomics, DNA methylomics, proteomics, and metabolomics on quiescent muscle stem cells from young and old mice. Our goals were to discover pathways that have been overlooked by isolated profiling approaches and to gain insight into which changes are causal, compensatory, correlational, and consequential. In our work, we found that glutathione metabolism is a key pathway of muscle stem cell aging that involves a compensatory feedback loop. Follow-up experiments showed that old muscle stem cells actually form a dichotomy between glutathione-high muscle stem cells and glutathione-low muscle stem cells. RNA-Seq showed that glutathione-high old muscle stem cells are able to synthesize adequate glutathione and thus compensate adequately for oxidative stress with increased glutathione turnover, while glutathione-low old muscle stem cells have failed to compensate for oxidative stress metabolically and instead show increased inflammatory signaling.
2023-03-20 | GSE152793 | GEO
Project description:To uncover new pathways that are important for skeletal muscle stem cell aging, we performed multiomics profiling, including transcriptomics, DNA methylomics, proteomics, and metabolomics on quiescent muscle stem cells from young and old mice. Our goals were to discover pathways that have been overlooked by isolated profiling approaches and to gain insight into which changes are causal, compensatory, correlational, and consequential. In our work, we found that glutathione metabolism is a key pathway of muscle stem cell aging that involves a compensatory feedback loop. Follow-up experiments showed that old muscle stem cells actually form a dichotomy between glutathione-high muscle stem cells and glutathione-low muscle stem cells. RNA-Seq showed that glutathione-high old muscle stem cells are able to synthesize adequate glutathione and thus compensate adequately for oxidative stress with increased glutathione turnover, while glutathione-low old muscle stem cells have failed to compensate for oxidative stress metabolically and instead show increased inflammatory signaling.
2023-03-20 | GSE152797 | GEO
Project description:Skeletal muscle holds an intrinsic capability of growth and regeneration both in physiological conditions and in case of injury. Chronic muscle illnesses, generally caused by genetic and acquired factors, lead to deconditioning of the skeletal muscle structure and function, and are associated with a significant loss in muscle mass. At the same time, progressive muscle wasting is a hallmark of aging. Given the paracrine properties of myogenic stem cells, extracellular vesicle-derived signals have been studied for their potential implication in both the pathogenesis of degenerative neuromuscular diseases and as a possible therapeutic target. In this study, we screened the content of extracellular vesicles from animal models of muscle hypertrophy and muscle wasting associated with chronic disease and aging. Analysis of the transcriptome, protein cargo and microRNAs (miRNAs) allowed us to identify a hypertrophic miRNA signature amenable for targeting muscle wasting, consisting of miR-1 and miR-208a. We tested this signature among others in vitro on mesoangioblasts (MABs), vessel-associated adult stem cells, and we observed an increase in the efficiency of myogenic differentiation. Furthermore, injections of miRNA-treated MABs in aged mice resulted in an improvement in skeletal muscle features, such as muscle weight, strength and cross-sectional area compared to controls. Overall, we provide evidence that the extracellular vesicle-derived miRNA signature we identified enhances the myogenic potential of myogenic stem cells.
2022-11-09 | PXD035446 | Pride
Project description:Aging is a complex multifactorial process leading to the loss of tissue/organ functionality and to an increase in disease risk. Aging-related intestinal dysfunctions include loss of barrier integrity, altered stress responses, nutrient malabsorption, and cancer formation. Many molecular mechanisms related to dysfunction and diseases are well-known (e.g. in cancer), however how aging impact on them before the occurrence of dysfunctions and diseases is poorly understood. In this study, we applied a multi-layered omics-approach to characterize the transcriptional and the epigenetic landscape of mouse intestinal epithelium during aging. We found gender and cell-type specific transcriptional and epigenetic alterations on key pathways and genes linked to intestinal dysfunctions, stem cell aging, organismal lifespan and cancer. Moreover, we identified a switch in the composition of the old intestinal stem cell subpopulations, represented by a drift towards a more secretory lineage committed (and less stem) state accompanied by functional epigenetic alterations.
2023-09-05 | GSE129710 | GEO
Project description:Aging is a complex multifactorial process leading to the loss of tissue/organ functionality and to an increase in disease risk. Aging-related intestinal dysfunctions include loss of barrier integrity, altered stress responses, nutrient malabsorption, and cancer formation. Many molecular mechanisms related to dysfunction and diseases are well-known (e.g. in cancer), however how aging impact on them before the occurrence of dysfunctions and diseases is poorly understood. In this study, we applied a multi-layered omics-approach to characterize the transcriptional and the epigenetic landscape of mouse intestinal epithelium during aging. We found gender and cell-type specific transcriptional and epigenetic alterations on key pathways and genes linked to intestinal dysfunctions, stem cell aging, organismal lifespan and cancer. Moreover, we identified a switch in the composition of the old intestinal stem cell subpopulations, represented by a drift towards a more secretory lineage committed (and less stem) state accompanied by functional epigenetic alterations.
2023-09-05 | GSE129708 | GEO
Project description:Aging is a complex multifactorial process leading to the loss of tissue/organ functionality and to an increase in disease risk. Aging-related intestinal dysfunctions include loss of barrier integrity, altered stress responses, nutrient malabsorption, and cancer formation. Many molecular mechanisms related to dysfunction and diseases are well-known (e.g. in cancer), however how aging impact on them before the occurrence of dysfunctions and diseases is poorly understood. In this study, we applied a multi-layered omics-approach to characterize the transcriptional and the epigenetic landscape of mouse intestinal epithelium during aging. We found gender and cell-type specific transcriptional and epigenetic alterations on key pathways and genes linked to intestinal dysfunctions, stem cell aging, organismal lifespan and cancer. Moreover, we identified a switch in the composition of the old intestinal stem cell subpopulations, represented by a drift towards a more secretory lineage committed (and less stem) state accompanied by functional epigenetic alterations.
2023-09-05 | GSE129510 | GEO