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

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

PROVIDER: PRJNA1039773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26807548.fastq.gz	Fastqsanger.gz
	SRR26807549.fastq.gz	Fastqsanger.gz
	SRR26807550.fastq.gz	Fastqsanger.gz
	SRR26807551.fastq.gz	Fastqsanger.gz
	SRR26807552.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]

2024-06-26 | GSE248603 | GEO

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 [RIP-seq]

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

| PRJNA1044835 | ENA

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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Sensing self and nonself circular RNAs

Project description:Circular RNAs (circRNAs) are single-stranded RNAs that are joined head to tail. Initially discovered as pathogen genomes such as hepatitis D virus (HDV) and plant viroids, circRNAs are recently recognized as a pervasive class of noncoding RNAs in eukaryotic cells, generated through back splicing. circRNAs have been postulated to function in cell-to-cell information transfer or memory due to their extraordinary stability. Whether and how circRNAs trigger immune recognition is not known. Here we show that exogenous circular RNAs potently stimulate immune signaling, and mammalian cells sense self vs. nonself circRNAs via circRNA biogenesis. Transfection of purified in vitro spliced circRNA into mammalian cells led to potent induction of innate immunity genes. The nucleic acid sensor RIG-I is necessary and sufficient to sense foreign circRNA, and RIG-I and foreign circRNA co-aggregate in cytoplasmic foci. CircRNA activation of innate immunity is independent of 5’ triphosphate, double-stranded RNA structure, or primary sequence of the foreign circRNA. Instead, self-nonself discrimination depends on the intron that programs the circRNA. Use of a human intron to express a foreign circRNA sequence abrogates immune activation, and the mature human circRNA is associated with diverse RNA binding proteins reflecting its endogenous splicing and biogenesis. These results reveal innate immune sensing of circRNA, a prevalent class of host and pathogen RNAs, and highlight introns—the predominant output of mammalian transcription—as unexpected arbiters of self-nonself identity in the RNA world.

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