Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rejuvenation of mesenchymal stem cells by human peripheral blood lymphocytes: A dual-mechanism for targeting senescent cell clearance and promoting cell proliferation in a coculture system [RNA-Seq]

ABSTRACT: Rejuvenation of mesenchymal stem cells by human peripheral blood lymphocytes: A dual-mechanism for targeting senescent cell clearance and promoting cell proliferation in a coculture system [RNA-Seq]

PROVIDER: PRJNA1314099 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Microarray data for rejuvenation experiments through reprogramming

Project description:Proliferative and replicative senescent fibroblasts from aged human donors were reprogrammed towards pluripotency and re-differentiated in fibroblasts and then further analyzed for rejuvenation assessment. Comparison of microarrays were performed by non hierarchical clustering visualized in with Treeview software

2011-12-14 | E-GEOD-27924 | biostudies-arrayexpress

Whole-Body Senescent Cell Clearance Alleviates Age-Related Brain Inflammation and Cognitive Impairment in Mice

Project description:Cellular senescence is characterized by an irreversible cell cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), which is a major contributor to aging and age-related diseases. Clearance of senescent cells has been shown to improve brain function in mouse models of neurodegenerative diseases. However, it is still unknown whether senescent cell clearance alleviates cognitive dysfunction during the aging process. To investigate this, we first conducted single-nuclei and single-cell RNA-seq in the hippocampus from young and aged mice. We observed an age-dependent increase in p16Ink4a senescent cells, which was more pronounced in microglia and oligodendrocyte progenitor cells and characterized by a SASP. We then aged INK-ATTAC mice, in which p16Ink4a-positive senescent cells can be genetically eliminated upon treatment with the drug AP20187 and treated them either with AP20187 or with the senolytic cocktail Dasatinib and Quercetin. We observed that both strategies resulted in a decrease in p16Ink4a exclusively in the microglial population, resulting in reduced microglial activation and reduced expression of SASP factors. Importantly, both approaches significantly improved cognitive function in aged mice. Our data provide proof-of-concept for senolytic interventions’ being a potential therapeutic avenue for alleviating age-associated cognitive impairment.

2021-02-06 | GSE161340 | GEO

Microarray data for rejuvenation experiments through reprogramming

2011-12-14 | GSE27924 | GEO

Combining Stem Cell Rejuvenation and Senescence Targeting to Synergistically Extend Lifespan

Project description:We combine transient stem cell rejuvenation with targeted removal of senescent cells to test the hypothesis that simultaneously targeting both cell-fate based aging mechanisms will maximize life and health span benefits.

2022-04-24 | GSE201338 | GEO

Clearance of p21-highly-expressing senescent cells accelerates wound healing

Project description:Clearance of p21-highly-expressing senescent cells accelerates wound healing

| PRJNA1168086 | ENA

Rejuvenation of mesenchymal stem cells by human peripheral blood lymphocytes-A dual-mechanism for targeting senescent cell clearance and promoting cell proliferation in a coculture system

Project description:Here we presented a novel approach to combat cellular senescence and promote cell proliferation by coculturing human MSCs with human peripheral blood lymphocytes (PBLs). In a heterogeneous population of MSCs comprising both aged and nonaged cells, PBL effector cells, rather than their cytokines, exhibited a dual role. They selectively induced apoptosis in aged cells by facilitating p53 SUMOylation and activating the p53-dependent mitochondrial pathway, while simultaneously safeguarding younger cells against senescence and promoting cell proliferation by activating Serpinb2/NF-κB signaling. This resulted in a decrease in aged MSCs and an enrichment of rejuvenated MSCs. This process effectively reversed the senescence phenotype, leading to the remodeling of stemness characteristics and the enhancement of functionality within the MSC population. Furthermore, MSCs rejuvenated by PBLs presented an enhanced therapeutic efficacy and a favorable safety profile.

| PXD066147 |

Rejuvenation of the aged brain immune cell landscape in mice through p16-positive senescent cell clearance.

Project description:Cellular senescence is a plausible mediator of inflammation-related tissue dysfunction. In the aged brain, senescent cell identities and the mechanisms by which they exert adverse influence are unclear. Here we used high-dimensional molecular profiling, coupled with mechanistic experiments, to study the properties of senescent cells in the aged mouse brain. We show that senescence and inflammatory expression profiles increase with age and are brain region- and sex-specific. p16-positive myeloid cells exhibiting senescent and disease-associated activation signatures, including upregulation of chemoattractant factors, accumulate in the aged mouse brain. Senescent brain myeloid cells promote peripheral immune cell chemotaxis in vitro. Activated resident and infiltrating immune cells increase in the aged brain and are partially restored to youthful levels through p16-positive senescent cell clearance in female p16-InkAttac mice, which is associated with preservation of cognitive function. Our study reveals dynamic remodeling of the brain immune cell landscape in aging and suggests senescent cell targeting as a strategy to counter inflammatory changes and cognitive decline.

| S-EPMC9515187 | biostudies-literature

Targeting PURPL RNA Enabled Rejuvenation of Senescence Cells via Epigenetic Reprogramming

Project description:Cellular senescence is a fundamental driver of ageing and age-related diseases, characterized by irreversible growth arrest and profound epigenetic alterations. While long non-coding RNAs (lncRNAs) have emerged as key regulators of senescence, their potential for senescent cell rejuvenation remains unexplored. Here, we identify the ageing-associated lncRNA PURPL as an epigenetic regulator that controls cellular rejuvenation through H3K9me3-mediated transcriptional silencing. CRISPRi-mediated PURPL depletion produces striking rejuvenation effects, resulting in restored youthful cell morphology, as well as suppression of senescence markers such as p21 and SA-β-gal. Conversely, PURPL overexpression accelerates cellular senescence, recapitulating the transcriptional and phenotypic hallmarks of ageing. Mechanistically, nuclear-localized PURPL regulates H3K9me3 deposition at 411 genomic loci including SERPINE1 (PAI-1) and EGR1, which are key senescence drivers. PURPL-mediated H3K9me3 loss at these loci derepresses their transcription, establishing a pro-senescence gene expression program. These findings reveal that PURPL is an epigenetic modulator of senescence and highlight its potential as a therapeutic target for age-related pathologies.

2025-10-27 | PXD068664 | Pride

Clearance of senescent macrophages ameliorates tumorigenesis in KRAS-driven lung cancer

Project description:Clearance of senescent macrophages ameliorates tumorigenesis in KRAS-driven lung cancer

| PRJNA957291 | ENA

Clearance of p21-highly-expressing senescent cells accelerates cutaneous wound healing

Project description:Clearance of p21-highly-expressing senescent cells accelerates cutaneous wound healing

| PRJNA1167732 | ENA