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Precision rescue of SP140 SNP+/+ Crohn's disease patient peripheral blood mononuclear cells responses to lipopolysaccharide using topoisomerase I or II inhibitors

ABSTRACT: Precision rescue of SP140 SNP+/+ Crohn's disease patient peripheral blood mononuclear cells responses to lipopolysaccharide using topoisomerase I or II inhibitors

PROVIDER: PRJNA675222 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13003946_1.fastq.gz	Fastqsanger.gz
	SRR13003946_2.fastq.gz	Fastqsanger.gz
	SRR13003947_1.fastq.gz	Fastqsanger.gz
	SRR13003947_2.fastq.gz	Fastqsanger.gz
	SRR13003948_1.fastq.gz	Fastqsanger.gz

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Precision rescue of SP140 SNP+/+ Crohn's disease patient peripheral blood mononuclear cells responses to lipopolysaccharide using topoisomerase I or II inhibitors

Project description:Peripheral blood-derived mononuclear cells isolated from Crohn's disease patients were pretreated with DMSO control, topotecan and etoposide and stimulated with LPS for 4 hours.

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Sp140 interactome analysis and proteomic analyis of WT vs Sp140 KO in Burkitt lynphoma

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [array]

Project description:Introduction: SP140 is a bromodomain/plant homeo domain (PHD)-containing reader with immune-restricted expression, and single nucleotide polymorphisms (SNPs) within SP140 associate with Crohn’s disease (CD). However, the function of SP140 and the consequences of disease-associated SP140 SNPs have remained unknown. Results: Individuals carrying CD-associated SNPs within SP140 had defective SP140 mRNA splicing, diminished SP140 protein, and severely suppressed innate immune signatures that stratified them from other CD patients. Conclusion: SP140 is a critical orchestrator of macrophage identity, and a loss of SP140 due to genetic variation contributes to a molecularly defined subset of CD characterized by suppressed innate immunity.

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [RNA-seq]

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [ChIP-seq]

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [ATAC-Seq]

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ChIP-seq analysis done for MBD3 before and after SP140 knockout in Ramos cells

Project description:Sp140 is a lymphocytic-restricted protein, an epigenetic reader working as a corepressor of genes implicated in inflammation and orchestrating macrophage transcriptional programs to maintain cellular identity. Reduced Sp140 expression is associated both to autoimmune diseases and blood cancer. However, the molecular mechanisms that link Sp140 altered protein levels to detrimental effects on the immune response and cellular growth, as well as the interactors through which Sp140 promotes gene silencing, remain elusive. In this work, we have applied a multi-omics approach (i.e. interactomics, ChIP-seq and proteomics) in two Burkitt lymphoma cell lines to identify both interactors and target genes of endogenous Sp140. We found that Sp140 interacts with the PRC2 and NuRD complexes and we demonstrated that Sp140 interaction with PRC2 is functional and directs H3K27me3 deposition on a set of target genes related to cellular growth and leukaemia progression.

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Selective inhibition of Homo sapiens M1 macrophages where SP140 mRNA is inhibited using siRNA

Project description:As part of our study in understanding the role of SP140 in inflammatory pathways in macrophages, we inhibited SP140 mRNA using siRNA. Peripheral blood mononuclear cells (PBMCs) were obtained from whole blood of healthy donors (from Sanquin Institute Amsterdam or from GSK Stevenage Blood Donation Unit) by Ficoll density gradient (Invitrogen). CD14+ monocytes were positively selected from PBMCs using CD14 Microbeads according to the manufacturer’s instructions (Miltenyi Biotec). CD14+ cells were differentiated with 20 ng/mL of macrophage colony-stimulating factor (M-CSF) (R&D systems) for 3 days followed by 3 days of polarization into classically activated (inflammatory) M1 macrophages (100 ng/mL IFN-γ; R&D systems). M1 macrophages were transfected with siGENOME human smartpool SP140 siRNA or non-targeting scrambled siRNA for 48h with DharmaFECT™ transfection reagents according to manufacturer’s protocol (Dharmacon). The cells were left unstimulated or stimulated with 100 ng/mL LPS (E. coli 0111:B4; Sigma) for 4h (for qPCR) or 24h (for Elisa). The cells were lysed (ISOLATE II RNA Lysis Buffer RLY-Bioline) for RNA extraction.150 ng total RNA was labelled using the cRNA labelling kit for Illumina BeadArrays (Ambion) and hybridized with Ref8v3 BeadArrays (Illumina). Arrays were scanned on a BeadArray 500GX scanner and data were normalized using quantile normalization with background subtraction (GenomeStudio software; Illumina). This submission only contains processed data

2022-07-22 | E-MTAB-12011 | biostudies-arrayexpress

H3K27me3 ChIP-seq in Burkitt lymphoma cells (Ramos cell line), wild type and SP140 knockout

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The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST [WT and SP140 KO RNA-seq]

Project description:Negative regulation of the antiviral cytokine IFN-I is critical to prevent host pathology, but is not fully understood. The highly conserved but understudied epigenetic reader and nuclear body protein SP140 represses IFN-I by an unknown mechanism. We describe the mechanism by which SP140 negatively regulates IFN-I, and include RNA-seq data of WT (B6) and SP140 KO BMMs untreated or treated with 100 ug/mL DMXAA for 8 hours in this dataset. We found that SP140 represses the expression of a novel positive regulator of IFN-I previously annotated as an annexin II receptor, which we rename RESIST (REgulated Stimulator of IFN-I via Stabilization of Transcript). RESIST promotes IFN-I mRNA stability by binding the CCR4-NOT mRNA deadenylase complex and blocking recruitment of the TTP family of RNA-binding proteins, which negatively regulate IFN-I mRNA stability, to CCR4-NOT. Mechanistically, RESIST uses N and C-terminal alpha-helices respectively to either dock to the CCR4-NOT complex or block TTP family binding. Our work reveals a new regulator of IFN-I and a new mechanism regulating IFN-I mRNA stability.

2024-08-28 | GSE269808 | GEO

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