Transcriptomics of THP-1 macrophages after treatment with NLRP3-induced EVs
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ABSTRACT:
PROVIDER: PRJNA749268 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15225600.fastq.gz | Fastqsanger.gz | |||
| SRR15225601.fastq.gz | Fastqsanger.gz | |||
| SRR15225602.fastq.gz | Fastqsanger.gz | |||
| SRR15225603.fastq.gz | Fastqsanger.gz | |||
| SRR15225604.fastq.gz | Fastqsanger.gz |
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Project description:Inflammasome, activated by pathogen-derived and host-derived danger signals, constitutes a multimolecular signaling complex that serves as a platform for caspase-1 (CASP1) activation and interleukin-1beta (IL1B) maturation. The activation of NLRP3 inflammasome requires two-step signals. The first “priming” signal (Signal 1) enhances gene expression of inflammasome components. The second “activation” signal (Signal 2) promotes the assembly of inflammasome components. Deregulated activation of NLRP3 inflammasome contributes to the pathological processes of Alzheimer’s disease (AD) and multiple sclerosis (MS). However, at present, the precise mechanism regulating NLRP3 inflammasome activation and deactivation remains largely unknown. By genome-wide gene expression profiling, we studied the molecular network of NLRP3 inflammasome activation-responsive genes in a human monocyte cell line THP-1 sequentially given two-step signals. We identified the set of 83 NLRP3 inflammasome activation-responsive genes. Among them, we found the NR4A nuclear receptor family NR4A1, NR4A2, and NR4A3, the EGR family EGR1, EGR2, and EGR3, the IkappaB family NFKBIZ, NFKBID, and NFKBIA as a key group of the genes that possibly constitute a negative feedback loop for shutting down inflammation following NLRP3 inflammasome activation. By molecular network analysis, we identified a complex network of NLRP3 inflammasome activation-responsive genes involved in cellular development and death, and immune and inflammatory responses, where transcription factors AP-1, NR4A, and EGR serve as a hub. Thus, NLRP3 inflammasome activation-responsive genes constitute the molecular network composed of a set of negative feedback regulators for prompt resolution of inflammation. To load the Signal 1 (S1), THP-1 cells were incubated for 3 hours in the culture medium with or without inclusion of 0.2 microgram/ml lipopolysaccharide (LPS). To load the Signal 2 (S2), they were incubated further for 2 hours in the culture medium with inclusion of 10 microM nigericin sodium salt dissolved in ethanol or the equal v/v% concentration of ethanol (vehicle), followed by processing for microarray analysis on Human Gene 1.0 ST Array (Affymetrix).
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Project description:THP-1 macrophages were treated with EVs and stimulated with LPS, and then total RNA was extracted from cells. Extracted total RNAs were investigated by microarray analysis. Increase and decrease of mRNA expression were investigated between EV-treated and non-treated THP-1 macrophages.
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2011-05-11 | E-GEOD-28785 | biostudies-arrayexpress
Project description:Purpose: The aim of this study was to obtain a comprehensive transcriptomic analysis of IL-26-exposed macrophages. Methods: THP-1 derived macrophage were generated by incubating THP-1 cells with PMA (50 ng/ml) for 24h.Then THP-1 macrophages were treated with IL-26 for 24h, which were collected and applied to RNA-sequencing. The constructed sequencing library was sequenced using an Illumina Novaseq 6000 system. The expression of transcripts was calculated as fragments per kilobase of exon model per million mapped reads (FPKM). Results: In total, we identified 1303 differentially expressed protein-coding genes between untreated and IL-26-treated macrophages, including 667 up-regulated and 636 down-regulated genes.
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Project description:The effect of SAA1 treatment on global gene expression in THP-1 macrophages was studied. The study determined the gene expression upon wild-type SAA1 treatment, variant SAA1 treatment (p.Gly72Asp) and in untreated THP-1 macrophages. SAA1 treatment of macrophages induces the expression of genes involved in inflammation, angiogenesis, phagocytosis and tissue remodeling which are important in the pathogenesis of chronic inflammatory diseases such as atherosclerosis and rheumatoid arthritis.
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Project description:Inflammasome, activated by pathogen-derived and host-derived danger signals, constitutes a multimolecular signaling complex that serves as a platform for caspase-1 (CASP1) activation and interleukin-1beta (IL1B) maturation. The activation of NLRP3 inflammasome requires two-step signals. The first “priming” signal (Signal 1) enhances gene expression of inflammasome components. The second “activation” signal (Signal 2) promotes the assembly of inflammasome components. Deregulated activation of NLRP3 inflammasome contributes to the pathological processes of Alzheimer’s disease (AD) and multiple sclerosis (MS). However, at present, the precise mechanism regulating NLRP3 inflammasome activation and deactivation remains largely unknown. By genome-wide gene expression profiling, we studied the molecular network of NLRP3 inflammasome activation-responsive genes in a human monocyte cell line THP-1 sequentially given two-step signals. We identified the set of 83 NLRP3 inflammasome activation-responsive genes. Among them, we found the NR4A nuclear receptor family NR4A1, NR4A2, and NR4A3, the EGR family EGR1, EGR2, and EGR3, the IkappaB family NFKBIZ, NFKBID, and NFKBIA as a key group of the genes that possibly constitute a negative feedback loop for shutting down inflammation following NLRP3 inflammasome activation. By molecular network analysis, we identified a complex network of NLRP3 inflammasome activation-responsive genes involved in cellular development and death, and immune and inflammatory responses, where transcription factors AP-1, NR4A, and EGR serve as a hub. Thus, NLRP3 inflammasome activation-responsive genes constitute the molecular network composed of a set of negative feedback regulators for prompt resolution of inflammation.
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