Effect of RIG-I activation and thymidine phosphorylase inhibition using Tipiracil on gene expression of human endothelial cells.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA842376 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
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| SRR19401886.fastq.gz | Fastqsanger.gz | |||
| SRR19401887.fastq.gz | Fastqsanger.gz | |||
| SRR19401888.fastq.gz | Fastqsanger.gz | |||
| SRR19401889.fastq.gz | Fastqsanger.gz | |||
| SRR19401890.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the role of RIG-I activation and thymidine phosphorylase inhibition human endothelial cells, we used a dsRNA agonist on HUVECs and HMVECs to activate RIG-I signaling, and further treated with tymp inhibitor TPI. We then performed differential gene expression analysis using data obtained from RNA-seq from each treatment group.
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Project description:Thymidine phosphorylase (TP) catalyzes the reversible phosphorolysis of thymidine, deoxyuridine, and their analogs to the respective bases and 2-deoxy-D-ribose-1-phosphate. TP is identical to platelet-derived endothelial cell growth factor (PD-ECGF). TP was reported to induce many angiogenic factors. However, the molecular mechanism of the TP function is still obscure. To elucidate the molecular basis for the TP function in human epidermoid carcinoma KB cells, we performed a whole genome-wide microarray analysis. Genes upregulated in KB cells overexpressing TP are supposed to represent potential molecular targets of TP in KB cells. KB cells (4 M-CM-^W 10^5) in 5 ml of culture media were cultured for 24 hours, then the growth medium was replaced with serum-free medium. These cells were maintained at 37 M-KM-^ZC in a humidified atmosphere of 5% CO2 for 12 hours, then these cells were collected for RNA extraction and quantification of the transcripts by microarray analysis.
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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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Project description:The RIG-I like receptor pathway is stimulated during RNA virus infection by interaction between cytosolic RIG-I and viral RNA structures that contain short hairpin dsRNA and 5M-bM-^@M-^Y triphosphate (5M-bM-^@M-^Yppp) terminal structure. In the present study, an RNA agonist of RIG-I was synthesized in vitro and shown to stimulate RIG-I-dependent antiviral responses at concentrations in the picomolar range. In human lung epithelial A549 cells, 5M-bM-^@M-^YpppRNA specifically stimulated multiple parameters of the innate antiviral response, including IRF3, IRF7 and STAT1 activation, andinduction of inflammatory and interferon stimulated genes - hallmarks of a fully functional antiviral response. Evaluation of the magnitude and duration of gene expression by transcriptional profiling identified a robust, sustained and diversified antiviral and inflammatory response characterized by enhanced pathogen recognition and interferon (IFN)signaling. Bioinformatics analysis further identified a transcriptional signature uniquely induced by 5M-bM-^@M-^YpppRNA, and not by IFNM-NM-1-2bthat included a constellation of IRF7 and NF-kB target genes capable of mobilizing multiple arms of the innate and adaptive immune response. Treatment of primary PBMCs or lung epithelial A549 cells with 5M-bM-^@M-^YpppRNA provided significant protection against a spectrum of RNA and DNA viruses. In C57Bl/6 mice, intravenous administration of 5M-bM-^@M-^YpppRNA protected animals from a lethal challenge with H1N1 Influenza, reduced virus titers in mouse lungs and protected animals from virus-induced pneumonia. Strikingly, the RIG-I-specific transcriptional response afforded partial protection from influenza challenge, even in the absence of type I interferon signaling. This systems approach providestranscriptional, biochemical, and in vivo analysis of the antiviral efficacy of 5M-bM-^@M-^YpppRNA and highlights the therapeutic potential associated with the use of RIG-I agonists as broad spectrum antiviral agents. A549 cells were either non-treated, treated with RNAiMax only, transfected with 5'pppRNA, or treated with IFNa-2b and analysed at 6h or 24h.
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