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

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

PROVIDER: PRJNA1044835 | ENA |

REPOSITORIES: ENA

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

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 | GSE248603 | GEO

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

2024-06-26 | GSE247585 | GEO

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

2024-06-26 | GSE247546 | 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 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 I

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

| PRJNA1039519 | ENA

Self-recognition of an inducible host lncRNA by RIG-I feedback restricts innate immune response

Project description:In this study, we employed a combination of UV-RIP-seq, PacBio-seq and iCLIP-seq technologies to identify long non-coding RNA associated with cytoplasmic RIG-I protein in mouse macrophages cells.

2018-04-26 | GSE106254 | GEO

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

The long noncoding RNA Lnczc3h7a promotes TRIM25-mediated RIG-I antiviral innate immune response

Project description:In this study, we employed a combination of RIP-seq and iCLIP-seq technologies to identify long non-coding RNA associated with cytoplasmic TRIM25 and RIG-I protein in mouse macrophages cells.

2019-03-12 | GSE112175 | GEO

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.

2017-06-29 | GSE81345 | GEO

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