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

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

PROVIDER: PRJNA683865 | ENA |

REPOSITORIES: ENA

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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 (heart)

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

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

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 (heart)

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

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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.

2024-02-14 | GSE225286 | GEO

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

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

Project description:Accumulation of senescent cells in the tumour microenvironment can drive tumourigenesis in a paracrine manner through the senescence-associated secretory phenotype (SASP). Using a new p16-FDR mouse line, we show that macrophages and endothelial cells are the predominant senescent cell types in murine KRAS-driven lung tumours. Single cell transcriptomics identify a population of tumour-associated macrophages, expressing a unique array of pro-tumourigenic SASP factors and surface proteins, that are also present in normal aged lungs. Genetic or senolytic ablation of senescent cells, and macrophage depletion, result in a significant reduction in tumour burden and increased mouse survival of KRAS-driven lung cancer models. Of translational relevance, we reveal the presence of macrophages with senescent features in human lung premalignant lesions, but not in adenocarcinomas. Together, our results have uncovered a population of senescent macrophages contributing to the initiation and progression of lung cancer, thus opening potential therapeutic avenues and cancer preventative strategies.

2023-06-02 | GSE230054 | GEO

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

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

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Clearance of a senescent macrophage-enriched niche ameliorates tumorigenesis in KRAS-driven murine lung cancer models

Project description:Understanding the important role of the tumour microenvironment on tumour initiation and progression is vital for a comprehensive understanding of cancer biology to design effective treatment strategies. Cellular senescence, while traditionally thought of as a cell autonomous tumour-suppressive response to potentially oncogenic insults, is now appreciated to have paracrine tumour promoting roles. We demonstrate a pro-tumourigenic effect of senescent microenvironmental cells on mouse lung tumour progression. To better understand the characteristics of these pro-tumourigenic senescent cells in the tumour microenvironment, we compare putatively senescent cells (reported by mCherry-expression) and non-senescent cells (mCherry-negative cells) from the lung microenvironment of mice induced to form lung tumours by oncogenic KrasG12D-expression in the lung epithelium. Putatively senescent cells are isolated by FACS, based on mCherry-expression which is expressed under the control of the Cdkn2a (p16) locus using a novel genetically engineered allele (p16FDR/+), along with their non-senescent counterparts for comparison by single cell RNA-sequencing.

2023-06-14 | GSE203447 | GEO

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