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Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Agilent)

ABSTRACT: Our systems analysis reported here demonstrates that TLR-responses in macrophages are markedly impaired by SHARPIN deficiency, and that SHARPIN controls expression of a subset of TLR2-induced, NF-kB and AP-1 dependent genes that overlaps with those affected by the hypomorphic panr2 mutation in NEMO. 46 total RNA samples from murine bone marrow derived macrophages were analyzed (32 by Agilent array, 14 by Affymetrix Exon array) On Agilent array, the responses of macrophages to 12hr stimulation with the TLR2 ligand PAM3CSK4 (300ng/mL) were analyzed in biological duplicates for five mutant mouse strains and respective controls: Sharpin(cpdm), Ikbkg(panr2), Atf3(KO), Il10(KO), and Nfkb1(KO).

ORGANISM(S): Mus musculus

SUBMITTER: Daniel Zak

PROVIDER: E-GEOD-29888 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Affymetrix)

Project description:Our systems analysis reported here demonstrates that TLR-responses in macrophages are markedly impaired by SHARPIN deficiency, and that SHARPIN controls expression of a subset of TLR2-induced, NF-kB and AP-1 dependent genes that overlaps with those affected by the hypomorphic panr2 mutation in NEMO. 46 total RNA samples from murine bone marrow derived macrophages were analyzed (32 by Agilent array, 14 by Affymetrix Exon array) On Affymetrix Exon array, the responses of macrophages to 12hr stimulation with the TLR2 ligand PAM3CSK4 (300ng/mL) were analyzed in biological duplicates for the Map3k8(sluggish) mutant and respective controls and in singlet for the Tnf(KO) mutant compared to two respective WT controls.

2011-08-30 | E-GEOD-29891 | biostudies-arrayexpress

Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses

Project description:This SuperSeries is composed of the following subset Series: GSE29888: Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Agilent) GSE29891: Systems analysis identifies an essential role for SHARPIN in macrophage TLR2 responses (Affymetrix) Refer to individual Series

2011-08-30 | E-GEOD-29947 | biostudies-arrayexpress

The role of Ch25h in the macrophage response to poly(I:C) (bone-marrow-derived macrophages)

Project description:Cross-talk between sterol regulatory pathways and inflammatory pathways has been demonstrated to play an important role in the response to viral infections. 25-Hydroxycholesterol (25HC) is an oxysterol that plays multiple roles in lipid biosynthesis and immunity, and has recently been shown to have anti-viral activity. Surprisingly, we found that deletion of Ch25h, the gene encoding the enzyme responsible for 25HC production, is protective in a mouse model of influenza infection as a result of decreased inflammatory-induced pathology. Anti-viral responses involve complex gene regulatory circuits with multiple feedback loops and we demonstrated that 25HC acts as an amplifier of TLR3 signaling in macrophages and airway epithelial cells. We determined that 25HC amplifies TLR3 signaling, at least in part, by mediating the up-regulation and recruitment of the AP1 components Fos and Jun to the promoters of a subset of TLR3 responsive genes. Thus, our study demonstrates for the first time that in addition to its direct anti-viral role, 25HC also regulates transcriptional responses and acts as an amplifier of TLR3-induced inflammation via AP1. 24 RNA samples from murine bone-marrow-derived macrophages were analyzed using Agilent microarrays. Macrophages from C57BL/6 and Ch25h-/- mice were analyzed after mock stimulation or stimulation with 6ug/mL poly(I:C) or for 6 or 18 hours. For each condition, three biological replicates (macrophages derived from independent mice) were analyzed.

2014-06-20 | E-GEOD-54062 | biostudies-arrayexpress

Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (microarray)

Project description:Macrophages, a key cellular component of inflammation, become functionally polarized in a signal- and context-specific manner. Th2 cytokines such as IL-4 polarize macrophages to a state of alternative activation that limits inflammation and promotes wound healing. Alternative activation is mediated by a transcriptional program that is influenced by epigenomic modifications including histone acetylation. To determine if Histone Deacetylase 3 (HDAC3) has a role in macrophage polarization including alternative activation, we have performed global gene expression analysis in macrophages with and without HDAC3 and with or without IL-4 exposure. From this data, we conclude that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4 induced alternative activation and furthermore are hyper-responsive to IL-4 stimulation. Mouse bone marrow derived macrophages were obtained from both control and HDAC3 KO animals and treated with vehicle control (BSA) or IL-4 for 24 hours. RNA was isolated and subjected to analysis using an Agilent Whole Genome Microarray Kit.

2011-11-10 | E-GEOD-33608 | biostudies-arrayexpress

Genome-wide microRNA expression induced by TNF

Project description:We sequenced microRNAs from bone marrow derived macrophages derived from the control (WT) and RBP-J conditional knockout mice (RBP-J KO; Rbpjf/f; LysM Cre). Examination of differential microRNA expression levels induced by TNF as well as regulated by RBP-J in bone marrow derived macrophages.

2016-07-22 | E-GEOD-72966 | biostudies-arrayexpress

MiR expression profile in M1-polarized bone marrow derived macrophage cells compared with normal mouse aortic tissue.

Project description:The global change of the miR expression profile during atherosclerosis is due to the infiltration of different types of leukocytes into the arterail vessel wall in addition to disease-specific regulation in vascular cells. Monocyte-derived macrophage accumulation in the subintimal region is critical in the formation of atherosclerotic plaques. It is currently unknown which miRs are involved in the atherogenic macrophage response. The comparison of the miR expression profile in LPS/Interferon-gamma activated mouse macrophages with the miR expression in the normal aortic vessel wall was performed to detect macrophage-enriched miRs. This screening may help to identify macrophage-enriched miRs in atherosclerotic vessels that may play a role in the macrophage function during atherogenesis. Bone marrow cells were harvested from femura of 6-8 week old female C57BL/6 mice, re-suspended in DMEM-F12/10% FCS/10% L929-conditioned medium, and cultured for 7 days to differentiate into primary macrophages. F4/80 and CD11b expression was determined by flow cytometry to confirm the macrophage phenotype. Macrophages were stimulated with LPS (100ng/ml, 14 hours) and INF-g (10ng/ml, 6 hours) and the M1 polarization was verified by quantification of mannose receptor C type 1 (MRC1), arginase II (ArgII), inducible nitric oxide synthase (iNOS), and arginase I (ArgI) by qRT-PCR. Total RNA (M1-type macrophages and aorta tissue) was isolated using mirVana microRNA Isolation Kit.

2014-01-01 | E-GEOD-26556 | biostudies-arrayexpress

DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

Project description:DNA damage response kinase ATM regulates the genetic program of lymphocytes with phsiologically induced DNA DSBs. In bone marrow-derived macrophages, related kinase DNAPKcs is also responsible for activating DNA damage responses after infection with Listeria monocytogenes. Here we show that both ATM and DNA-PKcs regulate the genetic program of Listeria monocytogenes-infected macrophages. Two independent bone marrow-derived macrophage cultures for each genotype (LysMcre/+ and Scid: Atmc/c: LysMcre/+) were infected with Listeria monocytogenes for 24 hrs at an MOI of 5. RNA was isolated using RNeasy (Qiagen). Gene expression profiling was performed using Illumina MouseRef-8 expression microarrays.

2015-07-03 | E-GEOD-70467 | biostudies-arrayexpress

Macrophage epoxygenase determines a pro-fibrotic transcriptomesignature

Project description:Epoxygenases belong to the cytochrome P450 family and they generate epoxyeicosatrienoic acids (EETs) known to have anti-inflammatory effects but little is known about their role in macrophage function. By high-throughput sequencing of RNA (RNA-seq) in primary macrophages derived fromrodents and humans, we establish the relative expression of epoxygenases in these cells. Zinc-finger nuclease-mediated targeted gene deletion of the major rat macrophage epoxygenase Cyp2j4 (orthologue of human CYP2J2),resulted inreduced EET synthesis. Cyp2j4-/-macrophages have relatively increased PPARγ levels and show a pro-fibrotic transcriptome,displayingover-expression of a specific subset of genes (260 transcripts) primarily involved in extracellular matrix, with fibronectin being the most abundantly expressed transcript.Fibronectin expression is under the control of epoxygenase activity in human and rat primary macrophages. In keeping with the invitro findings, Cyp2j4-/- rats show up-regulation of type I collagen following unilateral ureter obstruction (UUO) of the kidney and quantitative proteomics analysis (LC-MS/MS) showed increased renal type I collagen and fibronectin protein abundance resulting from experimentally induced crescentic glomerulonephritis in these rats. Taken together, these results identify the rat epoxygenase Cyp2j4 as a determinant of a pro-fibrotic macrophage transcriptome that could have implications in various inflammatory conditions depending on macrophage function. Gene expression profile generated for macrophages in wild type and Cyp2j4 KO WKY rats

2015-02-10 | E-GEOD-65715 | biostudies-arrayexpress

Transcription profiling of mouse classically activated and type II activated macrophages to identify novel markers

Project description:The purpose of this study is to identify novel markers for the type II activated macrophage, which is generated by classical stimulation in the presence if IgG immune complexes. These cells gererally produce high levels of IL-10 and low levels of IL-12, in comparison to classically activated macrophages. We wish to identify gene expression which is enriched in Type II activated macrophages in comparison to classically activated macrophages. Experiment Overall Design: The design of this experiment is to simulateously stimulate two popultions of macrophages and compare their gene expression. In this case, macrophages are primed overnight with IFN-gamma, washed, then stimulated with LPS (Classically) or LPS+Immune complexes (Type II).

2008-06-13 | E-GEOD-4811 | biostudies-arrayexpress

Nitric oxide modulates metabolic remodelling and immunometabolism in inflammatory murine macrophages

Project description:Classical stimulation of macrophages (MLPS/IFNγ) elicits the expression of inducible nitric oxide synthase (iNOS), generating large amounts of nitric oxide (NO) and inhibiting respiration. Consequent upregulation of glycolysis and a disrupted tricarboxylic acid (TCA) cycle underpin this switch to a pro-inflammatory phenotype. Here we show that the NOS cofactor tetrahydrobiopterin (BH4) modulates key aspects of metabolic remodelling in activated bone-marrow-derived macrophages (BMDMs) via NO production. Using two complementary mouse models that each lack the capacity for inducible NO generation, through different mechanisms, we reveal that NO regulates macrophage respiratory function via changes in the abundance of critical N-module subunits in Complex I, by HIF1α-mediated glycolytic remodelling, and by modulating levels of the critical TCA cycle metabolites, and inflammatory mediators, citrate, succinate, and itaconate. Taken together, our findings reveal new critical roles for iNOS-derived NO that are required for metabolic remodelling and cytokine production in macrophage inflammatory responses.

2019-05-31 | PXD010628 | Pride

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