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RNA-Sequencing Facilitates Quantitative Analysis of Control and Mettl3 Knockdown LPS-induced Macrophage Transcriptomes

ABSTRACT: RNA-Sequencing Facilitates Quantitative Analysis of Control and Mettl3 Knockdown LPS-induced Macrophage Transcriptomes

PROVIDER: PRJNA792268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17331222_1.fastq.gz	Fastqsanger.gz
	SRR17331222_2.fastq.gz	Fastqsanger.gz
	SRR17331223_1.fastq.gz	Fastqsanger.gz
	SRR17331223_2.fastq.gz	Fastqsanger.gz
	SRR17331224_1.fastq.gz	Fastqsanger.gz

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RNA-Sequencing Facilitates Quantitative Analysis of Control and Mettl3 Knockdown LPS-induced Macrophage Transcriptomes

Project description:The goal of this study is to investigate the potential role of Mettl3 in the innate immune response by RNA-seq

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METTL3 Deficiency in Macrophage Aggravates Neutrophilic Asthma by Regulating ZBP1-NLRP3 Inflammasome Activation

Project description:N6-methyladenosine (m6A), the most abundant RNA modification, plays the essential role in the immune disorders. Yet, the role of m6A and its master regulator, methyltransferase-like 3 (METTL3) in asthma remain ambiguous. Here, we found that macrophage deficient in METTL3 aggravates the ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma. Subsequently, we observed that METTL3 deficiency facilitates NLRP3 but not AIM2 and NLRC4-dependent inflammasome activation and IL-1β secretion. Mechanistically, METTL3 deficiency enhanced NLRP3 inflammasome activation were dependent on upregulation of ZBP1 and TRAF1. Lastly, we elucidated that METTL3 negatively regulates ZBP1 expression through m6A modification dependence. In summary, the study unveils the function of m6A in regulating NLRP3 inflammasome activation in macrophage and identifies potential targets in therapeutic intervention of neutrophilic asthma.

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TBK1-METTL3 axis facilitates antiviral immunity

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Next Generation Sequencing Facilitates Quantitative Analysis of dendritic cell Transcriptomes during LPS response

Project description:Purpose:The purpose of this study is to detect activated or silenced genes during LPS-induced dendritic cell. Gene expression differences between two samples could be found using transcriptome profiling (RNA-seq) analysis. Methods:Mouse dendritic cells were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse GM-CSF and IL-4, immature DCs were obtained before or after LPS stimulation. Immature DCs were sorted respectively based on marker CD86 and Iab(MHCII) using flowcytrometer. DC mRNA profiles were generated by deep sequencing,using Illumina. Results: We mapped about 10 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA variation during LPS stimulation. DC mRNA profiles immature BMDCs were generated by deep sequencing

2015-09-11 | E-GEOD-69256 | biostudies-arrayexpress

METTL3 Regulates LPS-Induced Inflammatory Response via the NOD1 Signaling Pathway

Project description:Inflammation is normally a protective response to defend and restore homeostasis; nonresolving inflammation is a major driver of immune disorders. N6-methyladenosine (m6A) is a prevalent mRNA modification that plays a crucial function in multiple biological processes. The effect of m6A on the immune response has recently been reported. However, the effect is unclear, and the results are contradictory. In this study, the expression of total m6A and the methyltransferase METTL3 decreased in LPS-stimulated macrophages. METTL3 knockdown significantly upregulated expression of proinflammatory cytokines, including TNF-α, IL-6 and NO. RNA sequencing analysis showed that the upregulated genes were enriched in inflammation-related signaling pathways and that the NOD-like receptor signaling pathway might be the target molecules of METTL3. METTL3 depletion resulted in upregulation of the NOD1 pathway without impacting NOD2. Moreover, the increase in proinflammatory cytokines induced by METTL3 knockdown was reversed by blocking the NOD1 pathway using the NOD-IN-1 and ML130 specific inhibitors. Mechanistically, METTL3 knockdown promoted the mRNA expression and stability of NOD1 and RIPK2, and the same results were detected in m6A-binding protein YTHDF1- or YTHDF2-silenced cells. All findings suggested that METTL3 depletion inhibits the degradation of NOD1 and RIPK2 mRNA mediated by YTHDF1 and YTHDF2, which upregulate the NOD1 pathway and subsequently promote the LPS-induced inflammatory response in macrophages.

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Next Generation Sequencing Facilitates Quantitative Analysis of LPS treated THP-1 cells' Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of LPS treated THP-1 cells' Transcriptomes

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Next Generation Sequencing Facilitates Quantitative Analysis of LPS treated THP-1 cells' Transcriptomes

Project description:In order to understand the consequences of the LPS from different bacterias, we analyzed RNA gene expression profiles in a human myeloid cell line THP-1 cells. RNA-seq transcriptome was analyzed in THP-1 cells treated with LPS from three bacteria B. fungorum, S. marcescens, and P. myrsinacearum.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and α7nAChR-/- Peritoneal macrophage Transcriptomes with Nicotine and/or LPS treatment

Project description:Purpose: The cholinergic anti-inflammatory pathway (CAP) links the nervous and immune systems and modulates innate and adaptive immunity. The goals of this study are to identify the new downstream signaling of α7nAChR in macrophages. Methods: Peritoneal macrophages isolated from α7nAChR+/+ and α7nAChR-/- mice were treated with nicotine (10 μM) and/or LPS (100 ng/ml), then RNA-seq was performed. Results: Genes were selected that had more than 4-fold relative gene expression in nicotine-treated cells compared to the control group (vehicle-treated). The same calculation was applied to nicotine+LPS-treated cells and LPS-treated cells and 264 genes were identified as genes commonly induced by nicotine based on these two comparisons. Then relative gene expression was compared between α7nAChR+/+- and α7nAChR-/- -derived cells. 18 genes were finally selected whose expressions are suppressed (<1/2) in α7nAChR-/- -derived peritoneal macrophages. Conclusions: Our study represents the first detailed analysis focused on the new downstream signaling of α7nAChR in macrophages, generated by RNA-seq technology. We newly revealed the important anti-inflammatory role of Hes1 in the CAP using some functional experiments.

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TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

Project description:TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

| PRJNA674508 | ENA