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IRF2 regulates macrophages apoptosis through a STAT1/3 and Caspase-1-dependent mechanism

ABSTRACT: Using microarray gene expression profiling of liver RNA samples rerived from IRF2+/+ and IRF2-/- mice treated with saline or LPS, we identified >40 genes that were significantly down-regulated in IRF2 -/- mice, including STAT3 which has been reported to regulate apoptosis. Keywords: compound treatment design

ORGANISM(S): Mus musculus

PROVIDER: GSE5907 | GEO | 2007/09/01

SECONDARY ACCESSION(S): PRJNA97341

REPOSITORIES: GEO

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IRF2 regulates macrophages apoptosis through a STAT1/3 and Caspase-1-dependent mechanism

Project description:Using microarray gene expression profiling of liver RNA samples rerived from IRF2+/+ and IRF2-/- mice treated with saline or LPS, we identified >40 genes that were significantly down-regulated in IRF2 -/- mice, including STAT3 which has been reported to regulate apoptosis. Keywords: compound treatment design We compared gene expression in IRF2+/+ and IRF2-/- mice treated with Saline or LPS for 3 or 6 hours. Two repeats were done for the LPS treatments. The total number of arrays is 6.

2007-09-01 | E-GEOD-5907 | biostudies-arrayexpress

Genome-wide maps of IRF2 targets

Project description:Using ChIP-seq technology, we tried to find out the whole genome targets for IRF2 in mouse colorectal cancer (CRC) cells. More than 7000 genes were defined as the target of IRF2.

2019-04-25 | GSE110175 | GEO

Differences in gene expression between WT and IRF2 KO cells

Project description:Gasdermin-D (GSDMD) is cleaved by caspase-1/4/11 in response to canonical and non-canonical inflammasome activation. Upon cleavage, GSDMD oligomerizes and forms membrane pores, resulting in IL-1Î² secretion, pyroptotic cell death and inflammatory pathologies including periodic fever syndromes and septic shock â a plague on modern medicine. The transcriptional machinery that drives the expression of GSDMD is unknown. Here we show that IRF2, a member of the interferon-regulatory factor (IRF) family, is essential for the transcriptional activation of GSDMD. A forward genetic screen with ethyl-N-nitrosourea (ENU)-mutagenized mice unequivocally linked IRF2 to inflammasome signaling. Indeed, GSDMD transcript levels were highly attenuated in Irf2â/â macrophages upon Irf2 deficiency in macrophages, endothelial cells, and multiple organs, corresponding to attenuated IL-1Î² secretion and inhibited pyroptosis. Mechanistically, IRF2 binds a previously uncharacterized site within the GSDMD promoter to directly drive GSDMD transcription for execution of pyroptosis in response to canonical and non-canonical inflammasome activation. Our data illuminate a prominent transcriptional mechanism for the expression of GSDMD, a key mediator of inflammatory pathologies.

2019-05-21 | GSE130195 | GEO

Gene expression profiling of mouse macrophages following IRF2 knockdown

Project description:We applied next-generation sequencing to investigate the gene expression profiles in mouse bone-marrow derived macrophages with or without IRF2 knockdown. We identified a number of differentially regulated genes in cells with IRF2 knockdown.

2017-11-18 | GSE106895 | GEO

Microarray of IRF2 overexpress in iKAP primary cultured cells (#3346)

Project description:We used microarrays to study the global gene expression and identified differentially expressed genes in IRF2-overexpressing 3346 iKAP cells, aiming to identify genes and pathways that are regulated by IRF2.

2019-04-25 | GSE109579 | GEO

IRF2 ChIP seq in mouse intestinal stem cells (ISCs)

Project description:To examine whether IRF2, a negative regulator of IFN signaling, constitutively represses IFN signaling by binding IFN-inducible gene loci in ISCs, we performed a genome-wide chromatin immunoprecipitation/DNA sequencing (ChIP-Seq) analysis of IRF2 in Lgr5 ISCs. We identified 381 binding peaks in these cells, including well-known IFN-inducible genes. Motif analysis showed significant enrichment of consensus-binding motifs for IRF transcription factors within these peaks. Within IRF2-occupied genes in ISCs, we identified 204 of experimentally validated IFN-inducible genes from Interferome database, and 10.8% of them were overlapped with the genes upregulated by type I IFN stimulation in ISCs. These findings indicated for the first time that IRF2 constitutively bound and repressed the sterile IFN signaling at the level of ISCs.

2020-07-21 | GSE137260 | GEO

Gene expression analysis of intestinal stem cells (ISCs) in Irf2 conditional deletion mice.

Project description:To analyze global gene-expression changes caused by IRF2 loss in ISCs, ISCs were prepared from Irf2fl/fl: Lgr5-EGFP-Ires-CreERT2(Irf2fl/fl: Lgr5ki) mice or Irf2fl/fl: Ah-Cre: Lgr5-EGFP-Ires-CreERT2 (Irf2AhcKO: Lgr5ki) mice 1 month after 5 consecutive days of βNF treatment. The Gene Ontology (GO) analysis indicated that the GO terms overrepresented among the genes upregulated in ISCs of βNF treated Irf2AhcKO: Lgr5ki mice compared with those of Irf2fl/fl: Lgr5ki mice included “immune system process”, “immune response”, and “cellular response to Interferon-beta”, all from the GOTERM_Biological Processes (BP) category. Because these GO_term inculded many IFN-inducibl genes, IFN signaling augumented in Irf2 deleted ISCs.

2020-07-21 | GSE137190 | GEO

Expression Profiling of Primary Human Proerythroblasts (ProEs) After IRF2, IRF6, and MYB shRNA Knockdown

Project description:IRF2, IRF6, and MYB are candidate regulators of human erythropoiesis. We here examine primary CD34+ hematopoietic stem/progenitor cells (HSPCs)-derived erythroid progenitors with control, IRF2, IRF6, or MYB shRNA lentiviral transduction prior to differentiation. Gene expression microarray profiling datasets for MYB shRNA and control shRNA were obtained from Gene Expression Omnibus (GEO) under accession number GSE25678. The data were analyzed together with the datasets obtained in this study. Primary maturing adult erythroblasts were generated ex vivo from CD34+ hematopoietic stem/progenitor cells (HSPCs) using a serum-free two-phase liquid culture system. CD34+ HSPCs were transduced with lentiviruses containing shRNAs against IRF2 or IRF6 gene, selected and differentiated to proerythroblasts (ProEs). Cells were harvested at day 5 of differentiated and total RNA were extracted. This was used to hybridize to Affymetrix expression arrays using the HG-U133 Plus 2.0 platform.

2012-10-05 | E-GEOD-36988 | biostudies-arrayexpress

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

Project description:The physiological stresses that diminish tissue stem-cell characteristics remain largely unknown. We previously reported that type I interferon (IFN), which is essential for host antiviral responses, is a physiological stressor for hematopoietic stem cells (HSCs) and that interferon regulatory factor-2 (IRF2), which attenuates IFN signaling, maintains the stemness of HSCs. Here, we explore the role of IRF2 in maintaining colonic epithelial stem cells (CoSCs). In mice with a conditional Irf2 deletion in the intestinal epithelium (hereafter Irf2ΔIEC mice), both the number and the organoid-forming potential of CoSCs was markedly reduced. Consistent with this finding, the ability of Irf2ΔIEC mice to regenerate colon epithelium after injury by dextran sodium sulfate (DSS) was severely impaired, independently of microbial dysbiosis. Mechanistically, CoSCs differentiated prematurely into transit-amplifying (TA) cells in Irf2ΔIEC mice, which might explain their low CoSC counts. A similar phenotype was induced in wild-type mice by repeated injections of low doses of poly(I:C), which induces type I IFN. Collectively, we demonstrated that chronic IFN signaling physiologically stresses CoSCs. This study provides new insight into the molecular mechanisms that maintain functional CoSCs throughout life.

2020-09-18 | GSE107142 | GEO

Oral STAT3 Inhibitor, TTI-101, in Patients With Advanced Cancers

Project description:Many patients have cancers that have increased activity of a protein called STAT3 that contributes critically to the development and growth of their cancer. Despite our knowledge of STAT3’s importance to cancer, scientists and doctors have not developed a drug that targets it and that patients can take to treat their cancer more effectively than treatments that are now available. Tvardi Therapeutics, Incorporated has developed a compound, TTI-101, which can be given by mouth and acts as a direct inhibitor of STAT3. Administration of TTI-101 to mice demonstrated that it blocked growth of cancers of the breast, head and neck, lung, and liver and it was safe when administered at high doses to mice, rats, and dogs. In this application, Tvardi is proposing to further develop TTI-101 for treatment of solid tumors for which the prognosis is dismal. The investigators will determine how safe it is when administered to patients with cancer, determine whether an adequate dose can be administered to patients with cancer that will block STAT3 in their cancer, and determine whether treatment with TTI-101 leads to reduced growth of their cancer.

| 2247646 | ecrin-mdr-crc

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