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Expression profile of p16High primary peritonal macrophages

ABSTRACT: In our laboratory, we developed a new knock-in murine model to trace p16 cells ex vivo using EGFP as a reporter gene under the control of the endogenous promoter (exon 3) of the p16 locus from the CDKN2A gene (p16-Cre/Rosa26-mtmg). We showed previously that cells positive for p16-EGFP accumulated during natural aging. We previously reported (Grosse et al, 2020) that among this cells, liver endothelial cells and macrophages from liver and other tissues are the main population going into p16 activation. We are now analyzing the characteristics of p16High tissue resident peritoneal macrophages to understant the roll they have during adulhood and aging.

ORGANISM(S): Mus musculus

PROVIDER: GSE268932 | GEO | 2025/01/01

REPOSITORIES: GEO

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Defined p16High senescent cell types are indispensable for mouse healthspan

Project description:The accumulation of senescent cells can drive many age-associated phenotypes and pathologies. Consequently, it has been proposed that removing senescent cells might extend lifespan. Here we generated two knock-in mouse models targeting the best-characterized marker of senescence, p16Ink4a. Using a genetic lineage tracing approach, we found that age-induced p16High senescence is a slow process that manifests around 10-12 months of age. The majority of p16High cells were vascular endothelial cells mostly in liver sinusoids (LSECs), and to lesser extent macrophages and adipocytes. In turn, continuous or acute elimination of p16High senescent cells disrupted blood–tissue barriers with subsequent liver and peri-vascular tissue fibrosis and health deterioration. Our data show that senescent LSECs are not replaced after removal and have important structural and functional roles in the aging organism. In turn, delaying senescence or replacement of senescent LSECs could represent a powerful tool in slowing down aging.

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Expression profile of p16High primary peritonal macrophages

Project description:Expression profile of p16High primary peritonal macrophages

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Gene expression profiles of p16high and p16low adipocyte progenitor cells in the gonadal adipose tissue of 18 month old mice [scRNA_Adipose]

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

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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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Defined p16High senescent cell types are indispensable for mouse healthspan

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