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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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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.

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 [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 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]

| 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

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

Osteocyte Egln1/Phd2 links oxygen sensing and biomineralization via FGF23

Project description:Osteocyte Egln1/Phd2 links oxygen sensing and biomineralization via FGF23

| PRJNA847602 | ENA

LGP2 binds PACT to regulate RIG-I- and MDA5-mediated antiviral response

Project description:The RIG-I-like receptors (RLRs: RIG-I, MDA5 and LGP2) trigger inflammatory and antiviral responses by sensing non-self RNA molecules produced during viral replication. LGP2 regulation of RIG-I and MDA5-dependant type-I interferon signaling is a matter of controversy. Here we show that LGP2 interacts with different components of the RNA silencing machinery. Particularly, we identified a direct protein-protein interaction between LGP2 and interferon-inducible double-stranded RNA-dependent protein kinase activator A (PACT). The LGP2-PACT interaction is mediated by the regulatory C-terminal domain of LGP2 and is necessary for inhibiting the RIG-I- and amplifying the MDA5-responses. We describe a point mutation within LGP2 that disrupts LGP2-PACT interaction and leads to the loss of LGP2 regulatory activity over RIG-I and MDA5. These results provide a model in which PACT-LGP2 interaction regulates RIG-I and MDA5 inflammatory response and allows cellular RNA silencing machinery to coordinate the innate immune response.

2019-10-02 | PXD013191 | Pride

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