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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

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

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

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

Macrophage epoxygenase determines a pro-fibrotic transcriptomesignature

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

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

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