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Single cell analysis of senescent cells of old p16-FDR mice (heart)

ABSTRACT: Single cell analysis of senescent cells of old p16-FDR mice (heart)

PROVIDER: PRJNA683861 | ENA |

REPOSITORIES: ENA

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Single cell analysis of senescent cells of old p16-FDR mice (heart)

Project description:We report the analysis of single cell based sequencing to understand the cellular and molecular heterogeneity of senescent cell populations in vivo in multiple organ types. The findings will help characterise the roles different cell types play during the aging process.

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Single cell analysis of senescent cells of old p16-FDR mice (kidney)

Project description:Single cell analysis of senescent cells of old p16-FDR mice (kidney)

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Single cell analysis of senescent cells of old p16-FDR mice (lung)

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Single cell analysis of senescent cells of old p16-FDR mice (kidney)

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Single cell analysis of senescent cells of old p16-FDR mice (lung)

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p16-dependent upregulation of PD-L1 impairs immunosurveillance of senescent cells [RNA-seq: Lung Epithelial Cells]

Project description:The accumulation of senescent cells promotes aging, but a molecular mechanism that senescent cells use to evade immune clearance and accumulate remains to be elucidated. Here, we report that p16-positive senescent cells upregulate the immune checkpoint protein programmed death-ligand 1 (PD-L1) to accumulate in aging and chronic inflammation. p16-mediated inhibition of CDK4/6 promotes PD-L1 stability in senescent cells via the downregulation of ubiquitin-dependent degradation. p16 expression in infiltrating macrophages induces an immunosuppressive environment that can contribute to an increased burden of senescent cells. Treatment with immunostimulatory anti-PD-L1 antibody enhances the cytotoxic T cell activity and leads to the elimination of p16, PD-L1-positive cells. Our study uncovers a molecular mechanism of p16-dependent regulation of PD-L1 protein stability in senescent cells and reveals the potential of PD-L1 as a target for treating senescence-mediated age-associated diseases.

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p16-dependent upregulation of PD-L1 impairs immunosurveillance of senescent cells [RNA-seq: Lung Alveolar Macrophages]

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Chronic social stress induces p16-mediated senescent cell accumulation in mice

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Gene expression profile of p16-induced senescence in normal human diploid fibroblasts.

Project description:Transcriptional profiling of p16-induced senescent human diploid fibroblasts compared with proliferating cells. TIG-3 ER-p16 cells (primary normal human diploid fibroblasts expressing a 4-hydroxytamoxifen(4-OHT) regulatable form of human p16) were cultured for 7 days with or without 4-OHT. Total RNA was isolated using TRIzol reagent and were analyzed using the hum

2014-04-10 | E-GEOD-49863 | biostudies-arrayexpress

P16 positive microglia population identified in the aged mouse brain

Project description:Senescent cells are in a state of permanent cell cycle arrest, which is mediated by the Cyclin Dependent Kinase (CDK)4/6 inhibitor p16. During ageing, p16-expressing (P16pos) cells accumulate in tissues and promote multiple age-related pathologies, including neurodegenerative diseases. We evaluated the accumulation and the phenotype of senescent cells in the aged brain with a transgenic reporter mouse (p16-3MR), which allows for isolation of P16poscells. First, we showed that the number of P16pos cells is significantly increased in old brains. Second, using bulk RNAseq, we demonstrated that P16pos cells express high levels of inflammatory and lysosomal genes. Third, using single-cell RNAseq, we identified P16pos brain cells as being primarily microglia. Interestingly, the transcriptional profile of P16pos microglia cells is distinct from cell type signatures associated with senescence or defined microglia populations. Taken together, our study provides evidence for the accumulation of a novel P16pos microglia population in the aging brain, which could result in loss of tissue homeostasis and contribute to brain dysfunction.

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