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Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

ABSTRACT: Macrophage-inducible C-type lectin (Mincle, Clec4e) is a pathogen sensor that recognizes pathogenic fungi and Mycobactrium tuberculosis. We perfomed microarray analysis using peritoneal macrophages stimulated with TDM, a mycobacterial cell wall glycolipid that is known to be a Mincle ligand. Many chemokine and cytokine genes were upregulated in wildtype macrophages stimulated with TDM. Upregulation of these genes were completely abolishd in Mincle KO macrophages. Peritoneal macrophages from WT and Mincle KO mice were stimulated with TDM or vehicle for 24 h (3 samples each). Microarray analysis was performed using Affymetrix Mouse 430 2.0.

ORGANISM(S): Mus musculus

SUBMITTER: Chikara Komiya

PROVIDER: E-GEOD-52338 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis.

Tanaka Miyako M Ikeda Kenji K Suganami Takayoshi T Komiya Chikara C Ochi Kozue K Shirakawa Ibuki I Hamaguchi Miho M Nishimura Satoshi S Manabe Ichiro I Matsuda Takahisa T Kimura Kumi K Inoue Hiroshi H Inagaki Yutaka Y Aoe Seiichiro S Yamasaki Sho S Ogawa Yoshihiro Y

Nature communications 20140919

In obesity, a paracrine loop between adipocytes and macrophages augments chronic inflammation of adipose tissue, thereby inducing systemic insulin resistance and ectopic lipid accumulation. Obese adipose tissue contains a unique histological structure termed crown-like structure (CLS), where adipocyte-macrophage crosstalk is known to occur in close proximity. Here we show that Macrophage-inducible C-type lectin (Mincle), a pathogen sensor for Mycobacterium tuberculosis, is localized to macrophag ...[more]

PMID: 25236782

Similar Datasets

Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

Project description:Macrophage-inducible C-type lectin (Mincle, Clec4e) is a pathogen sensor that recognizes pathogenic fungi and Mycobactrium tuberculosis. We perfomed microarray analysis using peritoneal macrophages stimulated with TDM, a mycobacterial cell wall glycolipid that is known to be a Mincle ligand. Many chemokine and cytokine genes were upregulated in wildtype macrophages stimulated with TDM. Upregulation of these genes were completely abolishd in Mincle KO macrophages.

2013-11-14 | GSE52338 | GEO

Card9 dependent activation of macrophages by TDB

Project description:Bone marrow derived macrophages from wt and card9 KO mice were stimulated with CpG, Curdlan or TDB, an analogon to the mycobacterial cord factor TDM for 48h, respectively. Keywords: card9 knockout, macropphage, TDB wt or card9 KO macrophages stimulated for 48h

2009-01-31 | E-GEOD-10530 | biostudies-arrayexpress

Card9 dependent activation of macrophages by TDB

2009-02-01 | GSE10530 | GEO

Mus musculus

Project description:Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

| PRJNA227446 | ENA

Combined phosphoproteome analysis of the response to mycobacterial cord factor reveals a dichotomy of Mincle-dependent and -independent signaling in macrophages

Project description:Sensing of Mycobacterium tuberculosis by the immune system relies on recognition by macrophages. Mycobacterial cord factor, trehalose-6,6’-dimycolate (TDM), is the most abundant cell wall glycolipid and binds to the C-type lectin receptor Mincle. To explore the kinase signaling linking the TDM-Mincle interaction to gene expression, we employed quantitative phosphoproteome analysis using dimethyl-labeling and high-resolution mass spectrometry. TDM caused upregulation of 6.7% and suppressed 3.8% of the 14k phospho-sites identified in 3727 proteins. Mincle-dependent phosphorylation was observed for several canonical players of CLR signaling (e.g. PLC, PKC), and was enriched for PKC and GSK3 kinase motifs. Mincle-dependent activation of the PI3K-AKT-GSK3 pathway contributed to TDM-induced inflammatory gene expression and required the PI3K regulatory subunit p85. Unexpectedly, a substantial fraction of TDM-induced phosphorylation was Mincle-independent, a finding which was paralleled by RNAseq-based transcriptome data. GO and pathway enrichment analysis of both datasets concurred in the requirement for Mincle in “innate immune response”. In contrast, Mincle-independent phosphorylation and transcriptome responses to TDM were linked to “cell cycle” and to the DNA damage response. Collectively, our global analyses show substantial reprogramming of macrophages by mycobacterial cord factor and reveal a dichotomy of Mincle-dependent and –independent signaling linked to distinct biological responses

2019-01-17 | PXD009513 | Pride

Expression data from peritoneal macrophages stimulated with lipid A

Project description:Setdb1 is one of the H3K9 methyltransferases and represses gene expression by H3K9 methylation. In an attempt to elucidate the role of Setdb1 in the TLR4-mediated inflammatory responses, we performed DNA microarray analysis using lipid A (the active component of LPS)-stimulated peritoneal macrophages from macrophage specific Setdb1 KO (KO) and WT mice. The genes upregulated by lipid A treatment in WT macrophages and further increased in KO macrophages contain many genes associated with interleukins and chemokines. Peritoneal macrophages from WT and KO mice were stimulated with lipid A 10 ng/ml or vehicle for 4 h. Microarray analysis was performed using Affymetrix Mouse 430 2.0.

2016-06-27 | E-GEOD-78153 | biostudies-arrayexpress

Combined phosphoproteome and transcriptome analysis of the macrophage response to mycobacterial cord factor reveals a dichotomy of MINCLE-dependent and -independent signaling

Project description:Immune sensing of Mycobacterium tuberculosis relies on recognition by macrophages. Mycobacterial cord factor, trehalose-6,6’-dimycolate (TDM), is the most abundant cell wall glycolipid and binds to the C-type lectin receptor (CLR) MINCLE. To explore the kinase signaling linking the TDM-MINCLE interaction to gene expression, we employed quantitative phosphoproteome analysis. TDM caused upregulation of 6.7% and suppressed 3.8% of the 14,000 phospho-sites identified on 3727 proteins. MINCLE-dependent phosphorylation was observed for canonical players of CLR signaling (e.g. PLCg, PKCd), and was enriched for PKCd and GSK3 kinase motifs. MINCLE-dependent activation of the PI3K-AKT-GSK3 pathway contributed to inflammatory gene expression and required the PI3K regulatory subunit p85a. Unexpectedly, a substantial fraction of TDM-induced phosphorylation was MINCLE-independent, a finding paralleled by transcriptome data. Bioinformatic analysis of both datasets concurred in the requirement for MINCLE for innate immune response pathways and processes. In contrast, MINCLE-independent phosphorylation and transcriptome responses were linked to cell cycle regulation. Collectively, our global analyses show substantial reprogramming of macrophages by TDM and reveal a dichotomy of MINCLE-dependent and -independent signaling linked to distinct biological responses.

2019-06-01 | GSE115322 | GEO

Expression data from peritoneal macrophages stimulated with lipid A

2016-06-27 | GSE78153 | GEO

Mouse peritoneal macrophages at 3.5 or 48 hours, 0,0.5 or 5 μg/ml Leukocyte cell-derived chemotaxin 2 (LECT2),gene expression array, two independent biological replicates

Project description:LECT2 is a liver derived cytokine and involved in many pathologic conditions, especially in immune regulation. To better understand cellular and molecular mechanisms of LECT2 in immune response, mouse peritoneal macrophages were isolated from mouse peritonaeum. After treatment with 0, 0.5 or 5 μg/ml of LECT2 for 3.5 or 48 hours, gene expression profile in mouse peritoneal macrophages was measured using gene expression array. Results showed that LECT2 treatment led to the enhancement of cytokines secretion and phagocytosis in peritoneal macrophages. Gene expression in mouse peritoneal macrophages isolated from mouse peritonaeum were measured after exposure to 0,0.5 or 5 μg/ml LECT2 for 3.5 or 48 hours using gene expression array. Two independent experiments were performed using different mice for each experiment for gene expression array analysis.

2011-12-13 | E-GEOD-33721 | biostudies-arrayexpress

Transcription profiling of mouse wild-type, NF-IL6KO and KI(LAP) PECs

Project description:PECs from wild-type, NF-IL6KO and KI(LAP) mice were stimulated with or without LPS+IFN-gamma for 12h. We used microarrays to check the difference of gene induction among wild type, KO and KI mice. Experiment Overall Design: Peritoneal macrophages were collected for RNA extraction and hybridization on Affymetrix microarrays.

2008-06-15 | E-GEOD-7649 | biostudies-arrayexpress

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