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Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors [bulk RNA-Seq]

ABSTRACT: Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors [bulk RNA-Seq]

PROVIDER: PRJNA1188066 | ENA |

REPOSITORIES: ENA

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Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors

Project description:Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors

| PRJNA1188163 | ENA

Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors [single cell RNA-Seq]

Project description:Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors [single cell RNA-Seq]

| PRJNA1188118 | ENA

Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors [bulk RNA-Seq]

Project description:Sarcopenia, the age-related loss of muscle mass and strength, is characterized by impaired muscle repair and increased deposition of fibrotic tissue. Yet, the specific role of individual cell types in the development of fibrosis remains poorly defined. Here, we report that aged muscle stem cells (MuSCs) directly instruct fibro-adipogenic progenitors (FAPs) to proliferate and adopt a fibrogenic phenotype. Polycomb Ezh2-/- or aged mice exhibited regenerative defects, FAP expansion, fibrosis, and elevated levels of MuSC-secreted interleukin 6 (IL-6) and Spp1/Osteopontin. In aged MuSCs, H3K27me3 erosion at the NF-kB gene correlated with increased expression and enhanced chromatin recruitment at the IL-6 and Spp1 genes, leading to their activation. Blocking IL-6 and Spp1 signaling in co-cultures of aged MuSC and FAPs, or aged mice, reduced FAP proliferation and muscle fibrosis. In summary, our results indicate that aged MuSCs instruct FAPs to proliferate and acquire a fibrogenic phenotype through a mechanism involving epigenetically-mediated derepression of NF-kB and increased activation of IL-6 and Spp1- both of which are potential pharmacological targets.

2025-08-22 | GSE282285 | GEO

Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors [single cell RNA-Seq]

2025-08-22 | GSE282315 | GEO

Aged muscle stem cells epigenetically drive the expansion of mesenchymal progenitors

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-22 | GSE282342 | GEO

Mass spectrometry analysis of mouse hematopoietic stem cells and their progenitors reveals differential expression within and between proteome and transcriptome throughout adult and aged hematopoiesis

Project description:mass spectrometry analysis of aged and adult hematopoietic stem cells, multipotent progenitors and oligopotent progenitors

2021-07-24 | PXD017442 | Pride

Epigenetic dysregulation in aged muscle stem cells drives mesenchymal progenitor expansion via IL-6 and Spp1 signaling [CUT&Run]

Project description:Sarcopenia, the age-related decline in muscle mass, strength, and function, is characterized by impaired muscle homeostasis, reduced regenerative potential of muscle stem cells (MuSCs), and increased fibrosis. Here, we report that aged MuSCs can autonomously instruct fibro-adipogenic progenitors (FAPs) to proliferate and acquire a fibrogenic phenotype, independent of other cell types. Both the Polycomb-deficient Ezh2-/- mouse model and aged mice exhibited defective regeneration, FAP expansion, fibrosis, and elevated secretion of interleukin 6 (IL-6) and Spp1/Osteopontin by MuSCs. In aged MuSCs, reduction of the histone H3K27me3 repressive mark at the Nfbk1 gene correlated with its increased expression, enhanced chromatin recruitment to the IL6 and Spp1 genes, leading to their activation. Pharmacological inhibition of IL-6 and Spp1 signaling in co-culture systems or in aged mice reduced FAP proliferation and muscle fibrosis. These findings indicate that epigenetic dysregulation of aged MuSCs contributes to aged-related muscle fibrosis.

2025-08-22 | GSE298889 | GEO

Senolytics improve the neurogenic potential of non-glial progenitors and neurorepair in the dorsal pallium of aged killifish independent of inflammation

Project description:With advancing age, senescent cells accumulate as they are not efficiently cleared by the immune system anymore. Via a senescence-associated secretory phenotype, chronic senescent cells alter the microenvironment, creating an unfavorable milieu for neurogenesis and neurorepair. Using an innovative and rapid aging model, the African turquoise killifish, we have previously demonstrated a dramatic decline in neurogenic potential of non-glial progenitors with age. Even after traumatic brain injury, progenitor proliferation and neuron production was very low in aged killifish in comparison to young adult killifish, and overall neurorepair was incomplete. In the present study, we validated if the senolytic cocktail dasatinib and quercetin (D+Q) could reboot the neurogenic output by clearing chronic senescent cells from the aged killifish brain to re-create the necessary supportive environment. Our results confirm that the aged killifish telencephalon holds a very high senescent cell burden, which we could diminish by short-term systemic D+Q treatment. As a consequence of D+Q administration, proliferation of non-glial progenitors increased and more new neurons were generated and migrated into the parenchyma after injury. Injury-induced inflammation and glial scarring, a phenomenon only seen in aged killifish, remained unaltered. Senolytic treatment with D+Q might thus hold promise for improving brain function in aged populations, and is especially interesting for reviving the neurogenic potential of an already aged central nervous system.

2023-07-20 | PXD036437 | Pride

Aged Hematopoietic Stem Cells Drive Aging-Associated Immune Remodeling

Project description:Aged Hematopoietic Stem Cells Drive Aging-Associated Immune Remodeling

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Robust Expansion of Human Pancreatic Progenitors by Small Molecules

Project description:Robust Expansion of Human Pancreatic Progenitors by Small Molecules

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