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RNA accumulation in aged endothelial cells links an interferon gene signature to cellular senescence

ABSTRACT: RNA accumulation in aged endothelial cells links an interferon gene signature to cellular senescence

PROVIDER: PRJNA672989 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12926905_1.fastq.gz	Fastqsanger.gz
	SRR12926905_2.fastq.gz	Fastqsanger.gz
	SRR12926906_1.fastq.gz	Fastqsanger.gz
	SRR12926906_2.fastq.gz	Fastqsanger.gz
	SRR12926907_1.fastq.gz	Fastqsanger.gz

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RNA accumulation in aged endothelial cells links an interferon gene signature to cellular senescence

Project description:RNA-seq was performed on early passage and senescent human retinal microvascular endothel cells (HRMECs), to determine transcriptomic changes. Replicative and Etoposide-induced senescent HRMECs senescence-associated gene signature and upregulation of an interferon related gene signature.

2023-10-27 | GSE160356 | GEO

RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature II

Project description:Senescent endothelial cells accumulate in blood vessels during aging and contribute to age-related cardiovascular disease. Identification of senescent cells is challenging as molecular changes are cell-type specific. Here, we established, benchmarked, and validated a new gene signature EndoSEN that pinpoints senescent endothelial cells. The EndoSEN signature was enriched for interferon stimulated genes (ISG) and correlated with the senescence-associated secretory phenotype (SASP) signature. SASP establishment is classically attributed to DNA damage and cGAS activation, but our results revealed a pivotal role for RNA accumulation and sensing. Mechanistically, we showed that endothelial senescence hallmarks include self-RNA accumulation, RNA sensor RIG-I upregulation, and an ISG signature. Moreover, a virtual model of RIG-I knockout in endothelial cells underscored senescence as an impacted pathway. We tested and confirmed that RIG-I knockdown was sufficient to extend the lifespan and decrease the SASP in endothelial cells. Our evidence suggests that targeting RNA sensing is a potential strategy to delay vascular aging.

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RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature I

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RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature [RIP-seq]

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RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature

Project description:RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature

| PRJNA1039768 | ENA

RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature I

Project description:RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature I

| PRJNA1039519 | ENA

RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature II

Project description:RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature II

| PRJNA1039773 | ENA

RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature [RIP-seq]

Project description:RIG-I sensing of self-RNA in aged endothelial cells links cellular senescence with an interferon gene signature [RIP-seq]

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Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype

Project description:We found histological evidence for increased abundance of iron accumulating cells in association with fibrotic lung, kidney, and heart diseases in mice and humans. We showed that inducing iron accumulation by intratracheal iron delivery in mice is a potent inducer of inflammation, cellular senescence, and fibrosis. The aim of this study has been to understand the single cell dynamics of iron accumulation and the mechanics that link it to in vivo senescence and to fibrogenesis. To get deeper insight into how different cell types respond to iron accumulation, we performed single nuclei RNA sequencing (snRNA-seq) of lungs from mice which received a single intratracheal dose of iron 2 or 6 days prior to analysis, or PBS 6days prior to analysis (control).

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A homeostatic switch causing glycerol-3-phosphate and phosphoethanolamine accumulation triggers senescence by rewiring lipid metabolism

Project description:<p>Cellular senescence affects many physiological and pathological processes and is characterized by durable cell cycle arrest, an inflammatory secretory phenotype and metabolic reprogramming. Here, by using dynamic transcriptome and metabolome profiling in human fibroblasts with different subtypes of senescence, we show that a homeostatic switch which results in glycerol-3-phosphate (G3P) and phosphoethanolamine (PEtn) accumulation links lipid metabolism to the senescence gene expression program. Mechanistically, p53-dependent glycerol kinase (GK) activation and post-translational inactivation of Phosphate Cytidylyltransferase 2-Ethanolamine (PCYT2) regulate this metabolic switch, which promotes triglyceride accumulation in lipid droplets and induces the senescence gene expression program. Conversely, G3P phosphatase (G3PP) and Ethanolamine-Phosphate Phospho-Lyase (ETNPPL)-based scavenging of G3P and PEtn acts in a senomorphic way by reducing G3P and PEtn accumulation. Collectively, our study ties G3P and PEtn accumulation to controlling lipid droplet biogenesis and phospholipid flux in senescent cells, providing a potential therapeutic avenue for targeting senescence and related pathophysiology.</p>

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