Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA322388 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells [RRBS]
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Project description:Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells [ERRBS]
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Project description:Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells
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Project description:Aged hematopoietic stem cells (HSCs) display myeloid-biased differentiation and reduced regenerative potential. In this study, we uncover that P-selectin (Selp) marks a subset of aged HSCs with reduced repopulation capacity. This population of HSCs expresses a prominent aging transcriptome. Overexpression of Selp in young HSCs impaired long-term reconstitution potential and repressed erythropoiesis. We show that IL-1β is elevated in aged bone marrow and administration of IL-1β induces expression of Selp and other aging-associated genes in HSCs. Finally, we demonstrate that transplantation of aged HSCs into young recipients restores a young-like transcriptome, specifically by repressing pro-inflammatory pathways, highlighting the important role of the bone marrow microenvironment in HSC aging.
2023-01-02 | GSE194273 | GEO
Project description:Proteostasis supports stemness and its loss correlates with the functional decline of diverse stem cell types. Here we identify that chaperone-mediated autophagy (CMA), a selective autophagy pathway, is necessary for the regenerative capacity of muscle stem cells (MuSCs) throughout life. We show that CMA is active in MuSCs, while genetic loss of CMA in MuSCs or failure of CMA in normally aged cells causes a proliferative impairment, resulting in defective skeletal muscle regeneration. Reactivation of CMA in old MuSCs boosts their proliferative capacity and improves their regenerative ability. Using comparative proteomics to identify CMA substrates, we uncovered actin cytoskeleton and glycolytic metabolism as key processes altered in aged mice and human MuSCs. Our findings reveal CMA to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in old age.
2025-10-17 | PXD059966 | Pride
Project description:Engrams are considered to be substrates for memory storage, and the functional dysregulation of the engrams leads to cognition impairment.However, the cellular basis for these maladaptive changes lead to the forgetting of memories remains unclear. Here we found that the expression of autophagy protein 7 (Atg7) mRNA was dramatically upregulated in aged DG engrams, and led to the forgetting of contextual fear memory and the activation of surrounding microglia.To determine mechanism by which autophagy in DG engrams activates the surrounding microglia, mice were co-injected AAV-RAM-Cre either with AAV-Dio-Atg7-Flag or AAV-Dio- EYFP in dorsal dentate gyrus to overexpress ATG7 in the DG memory engrams. Microglia were separated using magnetic-activated cell sorting and subjected to RNA-Seq in dorsal hippocampus .Bioinformatics analysis shown overexpression of Atg7 in dorsal DG memory engrams caused an increase in the expression of Tlr2 in the surrounding microglia.Depletion of Toll-like receptor 2/4 (TLR2/4) in DG microglia prohibited excessive microglial activation and synapse elimination induced by the overexpression of ATG7 in DG engrams, and thus prevented forgetting. Furthermore, the expression of Rac1, a Rho-GTPases which regulates active forgetting in both fly and mice, was upregulated in aged engrams. Optogentic activation of Rac1 in DG engrams promoted the autophagy of the engrams, the activation of microglia, and the forgetting of fear memory. Invention of the Atg7 expression and microglia activation attenuated forgetting induced by activation of Rac1 in DG engrams. Together, our findings revealed autophagy-dependent synapse elimination of DG engrams by microglia as a novel forgetting mechanism.
2021-08-24 | GSE169019 | GEO
Project description:Proteostasis supports stemness and its loss correlates with the functional decline of diverse stem cell types. Here we identify that chaperone-mediated autophagy (CMA), a selective autophagy pathway, is necessary for the regenerative capacity of muscle stem cells (MuSCs) throughout life. We show that CMA is active in MuSCs, while genetic loss of CMA in MuSCs or failure of CMA in normally aged cells causes a proliferative impairment, resulting in defective skeletal muscle regeneration. Reactivation of CMA in old MuSCs boosts their proliferative capacity and improves their regenerative ability. Using comparative proteomics to identify CMA substrates, we uncovered actin cytoskeleton and glycolytic metabolism as key processes altered in aged mice and human MuSCs. Our findings reveal CMA to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in old age.
2025-10-15 | GSE286877 | GEO