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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 (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)

Project description: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 (heart)

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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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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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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

High p16⁺ senescence load confers increased responsiveness to senolytic therapy in aged female mice

Project description:Aging is accompanied by the accumulation of senescent cells, which contributes to tissue dysfunction and chronic inflammation. However, the burden of senescent cells and the efficacy of their clearance may differ between sexes, which is a critical yet understudied aspect of geroscience. Here, we combined transcriptomic, proteomic, and functional analyses to investigate sex-specific accumulation and removal of p16⁺ senescent cells during aging. Using single-nucleus and bulk RNA-seq, senescence-specific GLF16 staining, and bioluminescence imaging, we showed that aged female mice accumulated a higher burden of p16⁺ cells across multiple tissues, particularly the liver. Targeted elimination of p16⁺ cells via ganciclovir (GCV) in the p16-3MR mouse model resulted in significant improvements in physical performance, liver function, and skin regeneration in females but not in males. Multi-omics profiling revealed that p16⁺ cell clearance in females reprograms liver tissue toward a more youthful state, characterized by the upregulation of mitochondrial pathways and downregulation of immune and inflammatory signatures. These molecular changes closely mirror those induced by established longevity interventions such as calorie restriction, rapamycin, and acarbose. Moreover, integrative analysis across independent senescence-targeting studies identified a core set of conserved transcriptional regulators and gene targets, including Srm, Cd36, and Lrrfip1, which are involved in mitochondrial health and immune modulation. Together, our findings highlight the sex-specific benefit of senescent cell clearance in aging and provide mechanistic insight into the rejuvenating effects of targeting p16⁺ cells, supporting their potential as therapeutic targets in age-related diseases.

2026-01-21 | GSE297990 | GEO

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