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

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

PROVIDER: PRJNA1039519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26799249.fastq.gz	Fastqsanger.gz
	SRR26799250.fastq.gz	Fastqsanger.gz
	SRR26799251.fastq.gz	Fastqsanger.gz

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

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.

2024-06-26 | GSE247546 | GEO

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

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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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-26 | GSE247586 | GEO

Targeting a key disulfide linkage to regulate RIG-I condensation and cytosolic RNA-sensing

Project description:Maintaining innate immune homeostasis is critical for preventing infections and autoimmune diseases, but the effective interventions are lacking. Here, we identified Cys864-Cys869-mediated intermolecular disulfide-linkage formation as a critical step for human RIG-I activation that can be bidirectionally regulated to control innate immune homeostasis. The viral-stimulated Cys864-Cys869 disulfide-linkage mediates conjugation of an SDS-resistant RIG-I oligomer, which prevents RIG-I degradation by E3 ubiquitin-ligase MIB2 and is necessary for RIG-I to perform liquid-liquid phase separation to compartmentalize downstream signalsome, thereby stimulating IFN-I signaling. The corresponding C865S ‘knock-in’ caused defect of oligomerization and LLPS in mouse RIG-I, which inhibited innate immunity, resulting in increased viral load and mortality in mice. Through generating covalent Cys864-Cys869 linkage by unnatural amino-acid and developing interfering peptide to block Cys864-Cys869 residues, we bidirectionally regulate RIG-I activities in human diseases. These findings provide novel and in-depth insights on mechanism of RIG-I activation, develop methodologies that hold promising implications in clinics

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