Single cell RNA seq of hepatic and renal p16 positive cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA648934 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12331536_1.fastq.gz | Fastqsanger.gz | |||
| SRR12331536_2.fastq.gz | Fastqsanger.gz | |||
| SRR12331537_1.fastq.gz | Fastqsanger.gz | |||
| SRR12331537_2.fastq.gz | Fastqsanger.gz | |||
| SRR12331538_1.fastq.gz | Fastqsanger.gz |
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Project description:We performed the single cell RNA sequencing of mouse normal kidney, normal liver, and NASH-induced liver from p16-tdTomato mice. In order to enrich p16 positive cells, we independently sorted the non-separated cells (including both of p16 positive and negative cells) and p16 positive cells alone through tdTomato intensity by FACS. By obtaining 13,876 single cell transcripts, after the graph-based clustering and marker genes defined cell type classification, we identified the heterogeneity of in vivo p16-positive cells which dispersedly existed in renal cells and non-parenchymal hepatic cells. Differential expressing genes (DEGs) comparisons for each cell type were feasible to study the in vivo p16 dependent transcriptomic pattern change. Finally, we verified several cell type specific senescence-like phenotypes which were previously found on in vitro cellular senescence, and also identified the p16-related subpopulation which might involve in NASH progression and renal damage response.
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Project description:*Objectives:* In addition to their well-known role in the control of cellular proliferation and cancer, cell cycle regulators are increasingly identified as important metabolic modulators. Genome wide association studies identified SNPs near the cell cycle regulator CDKN2A/p16INK4a (p16) as strongly associated with risk of developing type 2 diabetes (T2D). T2D is associated with numerous perturbations of hepatic lipid and glucose metabolism. We have recently shown that p16 controls fasting-induced hepatic gluconeogenesis in mice. However, whether p16 may also affect hepatic lipid homeostasis is unknown. *Results:* In primary hepatocytes, p16-deficiency was associated with elevated expression of genes involved in fatty acid catabolism and enhanced activation of PPAR. This led to increased mitochondrial fatty acid oxidation (FAO) through a mechanism requiring the catalytic AMPK 2 subunit and SIRT1. By contrast, *p16* overexpression was associated with triglyceride accumulation and increased lipid droplet numbers *in vitro*, and decreased ketogenesis and hepatic mitochondrial activity *in vivo*. Gene expression analysis of human liver samples revealed a negative correlation between *CDKN2A* expression and *PPARA* and its target genes, suggesting a potential association between hepatic p16 expression and FAO in obese humans. *Conclusions:* Our findings demonstrate that p16 plays a key role in hepatic lipid metabolism and may thus contribute to the development of metabolic diseases.
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Project description:P16 positive microglia population identified in the aged mouse brain
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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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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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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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