Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression Data from murine control and IL6ralpha-deficient macrophages stimulated with Interleukin-6

ABSTRACT: IL-6 induces IL4ralpha expression in macrophages. This mechanism is necessary to promote macrophage polarization towards an M2-phenotype and is crucial to limit the inflammatory response both upon obesity and LPS-endotoxemia. In this dataset, we include the expression data obtained from primary murine bone marrow-derived macrophages from control and IL6ralpha-deficient macrophages (n=4vs4) stimulated with interleukin-6 (IL-6) 8 samples were analyzed to compare control and IL6ralpha-deficient macrophages for their gene expression profiles upon stimulation with IL-6

ORGANISM(S): Mus musculus

SUBMITTER: Jan Mauer

PROVIDER: E-GEOD-47426 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Signaling by IL-6 promotes alternative activation of macrophages to limit endotoxemia and obesity-associated resistance to insulin.

Mauer Jan J Chaurasia Bhagirath B Goldau Julia J Vogt Merly C MC Ruud Johan J Nguyen Khoa D KD Theurich Sebastian S Hausen A Christine AC Schmitz Joel J Brönneke Hella S HS Estevez Emma E Allen Tamara L TL Mesaros Andrea A Partridge Linda L Febbraio Mark A MA Chawla Ajay A Wunderlich F Thomas FT Brüning Jens C JC

Nature immunology 20140330 5

Obesity and resistance to insulin are closely associated with the development of low-grade inflammation. Interleukin 6 (IL-6) is linked to obesity-associated inflammation; however, its role in this context remains controversial. Here we found that mice with an inactivated gene encoding the IL-6Rα chain of the receptor for IL-6 in myeloid cells (Il6ra(Δmyel) mice) developed exaggerated deterioration of glucose homeostasis during diet-induced obesity, due to enhanced resistance to insulin. Tissues ...[more]

PMID: 24681566

Similar Datasets

Capacity of yolk sac macrophages, fetal liver and adult monocytes to colonize an empty niche and develop into functional tissue resident macrophages

Project description:Tissue-resident macrophages can derive from yolk sac macrophages, fetal liver monocytes or adult bone marrow monocytes. Whether these precursors can give rise to transcriptionally identical alveolar macrophages is unknown. Here, we transferred traceable yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages as a control, into the empty alveolar macrophage niche of neonatal Csf2rb-/- mice. All precursors efficiently colonized the alveolar niche and generated alveolar macrophages that were transcriptionally almost identical, with only 22 genes that could be linked to their origin. Underlining the physiological relevance of our findings, all transfer-derived alveolar macrophages self-maintained within the lungs for up to 1 year and durably prevented alveolar proteinosis. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages. CD45.1+CD45.2+ yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages from the bronchoalveolar lavage were sorted from wild type CD45.1+CD45.2+ mice of indicated ages. From part of these samples RNA was isolated. The other part was transferred intranasally into the lungs of neonate Csf2rb-/- mice. 6 weeks post-transfer, transfer-derived CD45.1+CD45.2+ alveolar macrophages were sorted from the bronchoalveolar lavage. Wild type CD45.1+CD45.2 alveolar macrophages from the bronchoalveolar lavage of 6 week old mice were sorted as control. 36 samples (arrays) in total. RNA was isolated, amplified with Nugene pico kit, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

2016-03-01 | E-GEOD-76999 | biostudies-arrayexpress

Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells

Project description:Self-renewing tissue-resident macrophages are thought to be exclusively derived from embryonic progenitors. However, whether circulating monocytes can also give rise to such macrophages has not been formally investigated. Here we use a new model of diphtheria toxin-mediated depletion of liver-resident Kupffer cells to generate niche availability and show that circulating monocytes engrafted in the liver, gradually adopt the transcriptional profile of their depleted counterparts and become long-lived self-renewing cells. Underlining the physiological relevance of our findings, circulating monocytes also contribute to the expanding pool of macrophages in the liver shortly after birth, when macrophage niches become available during normal organ growth. Thus, like embryonic precursors, monocytes can and do give rise to self-renewing tissue-resident macrophages if the niche is available to them. Clec4F+ Kupffer cells were isolated and sorted from livers from adult WT mice or KC-DTR or KC-DTR littermate control mice +/- 50ng DT at indicated timepoints. 19 samples (arrays) in total. RNA was isolated, amplified with Nugene pico kit, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

2015-11-21 | E-GEOD-75225 | biostudies-arrayexpress

p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer.

Project description:Anaplastic thyroid carcinoma (ATC) has among the worst prognosis of any solid malignancy. The low incidence of the disease has in part precluded systematic clinical trials and tissue collection, and there has been little progress in developing effective therapies. BRAF and TP53 mutations co-occur in a high proportion of ATC, particularly those associated with a precursor papillary thyroid carcinoma (PTC). In order to develop an adult-onset model of BRAF-mutant anaplastic thyroid carcinoma, we generated a novel thyroid-specific CreER transgenic mouse. We utilize a Cre-regulated BrafV600E mouse and a conditional Trp53 allelic series to demonstrate that p53 constrains progression from papillary to anaplastic thyroid carcinoma. Gene expression and immunohistochemical analyses of murine tumors identified the cardinal features of human ATC including loss of differentiation, local invasion, distant metastasis and rapid lethality. We employed small animal ultrasound imaging to monitor autochthonous tumors, and show that treatment with the selective BRAF inhibitor PLX4720 improved survival, but did not lead to tumor regression or suppress signaling through the MAPK pathway. Combination of PLX4720 and the MEK inhibitor PD0325901 more completely suppressed MAPK pathway activation in mouse and human ATC cell lines, and improved the structural response and survival of ATC-bearing animals. This model expands the limited repertoire of autochthonous models of clinically aggressive thyroid cancer, and these data suggest that small molecule MAPK pathway inhibitors hold clinical promise in the treatment of advanced thyroid carcinoma. Total RNA from five murine papillary thyroid carcinoma (PTC) tumors and five murine anaplastic thyroid carcinoma (ATC) tumors was analyzed.

2014-04-02 | E-GEOD-55933 | biostudies-arrayexpress

Expression data of IL-18 generated murine NK cells

Project description:We analyzed gene expression profiles of IL-18 generated murine NK cells in comparison to unstimulated, freshly isolated splenic NK cells. We identified a set of 1414 Affymetrix probe sets showing significant misregulation (Welch's T-test, p<0.05; Benjamini-Hochberg FDR corrected). IL-18 generated as well as unstimulated NK cells were isolated in three independent preparations and used for RNA extraction and hybridization on Affymetrix microarrays.

2012-07-10 | E-GEOD-33627 | biostudies-arrayexpress

ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains seven sets of exression array data. For all sample, we use four CEL files generated by four biological-independent experiments.

2015-08-31 | E-GEOD-71111 | biostudies-arrayexpress

Expression data in mouse primary mammary tumors

Project description:Many preclinical therapy studies have focused on a small number of well-described mouse allograft or human xenograft models that poorly represent the heterogeneity of human disease. Here we have assembled a panel of mouse mammary cell lines that metastasize in syngeneic mouse hosts and we have assessed gene expression programs in the untreated primary tumors with the goal of generating information that may be useful to the identification of biomarkers that predict response to therapeutic intervention. We used microarrays to assess global gene expression programs in primary tumors from 12 metastatic mouse mammary tumor models transplanted orthotopically into syngeneic, fully immunocompetent mouse hosts. The 12 tumor models used here are based on published cell lines that had been established from either spontaneous mammary tumors or from mammary tumors arising in genetically engineered mouse models. All cell lines were previously described to be metastatic. Cells were surgically implanted in the #4 mammary fat pads of syngeneic mice and primary tumors were harvested when they reached 0.5-1.0 cm diameter and snap-frozen for later RNA extraction. 4 independent tumors were collected for each of the 12 models.

2015-05-19 | E-GEOD-69006 | biostudies-arrayexpress

Gene Array Analyzer (GAA): Alternative usage of gene arrays to study alternative splicing events (MoGene array)

Project description:The latest version of microarrays released by Affymetrix, the GeneChip Gene 1.0 ST Arrays (gene arrays), are designed in a similar fashion as exon arrays, which enables to identify differentially expressed exons, rather than only the expression level of whole transcripts. Here, we propose an extension, Gene Array Analyzer (GAA), to our previously published Exon Array Analyzer (EAA). GAA enables to analyse gene arrays on exon level and therefore supports to identify alternative splicing with gene arrays. To show the applicability of GAA, we used gene arrays to profile alternative splice events during the development of the heart. Further re-analysis of published gene arrays could show, that some of these splice events reoccur under pathological conditions. The web interface of GAA is user friendly, functional without set up and freely available at http://GAA.mpi-bn.mpg.de. Alternative splicing and gene expression analysis during development of the heart and cardiomyoyte differentiation.

2011-11-28 | E-GEOD-30429 | biostudies-arrayexpress

Expression data from striatum of a mouse model of Huntington´s disease (HD) (HdhQ111/Q111) crossed with mGluR5 knockout mice (mGluR5-/-) and their respective controls (HdhQ20/Q20 and mGluR5+/+).

Project description:To try to investigate the mechanism behind the adaptive phenotypes observed in a mice model model of HD crossed with mGluR5 knockout, we analyzed whether mutated huntingtin (Htt) expression in a mGluR5 null background could be altering the expression of genes that might be involved in the pattern of Htt aggregation and HD-related locomotor alterations. In this data set, we include analysis of gene expression in striatum of mice with four different genotypes: HdhQ20/Q20/mGluR5+/+; HdhQ20/Q20/mGluR5-/- ; HdhQ111/Q111/mGluR5+/+ ; HdhQ111/Q111/mGluR5-/- 12 samples were analyzed. We used Partek Genomics Suite v6.5 (Partek, St. Louis, MO) to determine differences in gene expression levels. Genotype effects were considered significant based of the following criteria: (i) ANOVA p-values< 0.05 and (ii) 1.5 fold increase or decrease.

2013-08-28 | E-GEOD-50379 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [array]

Project description:In immune responses, activated T cells migrate to B cell follicles and develop to T follicular helper (Tfh) cells, a new subset of CD4+ T cells specialized in providing help to B lymphocytes in the induction of germinal centers 1-3. Although Bcl6 has been shown to be essential in Tfh cell function, it may not regulate the initial migration of T cells 4 or the induction of Tfh program as exampled by CXCR5 upregulation 5. Here, we show that the Achaete-Scute homologue 2 (Ascl2) gene that encodes a basic helix-loop-helix (bHLH) transcription factor 6, is selectively upregulated in its expression in Tfh cells. Ectopic expression of Ascl2 uniquely upregulates CXCR5 but not Bcl6 and downregulates CCR7 expression in T cells in vitro and accelerates T cell migration to the follicles and Tfh cell development in vivo. Combined transcriptome profiling and genome-wide occupancy analysis indicate that Ascl2 directly regulates Tfh-related genes while inhibits expression of Th1 and Th17 genes. Acute deletion of Ascl2 as well as blockade of its function with the Id3 protein in peripheral CD4+ T cells results in a failure in Tfh cell development and the germinal center response. Conversely, mutation of Id3, known to cause antibody-mediated autoimmunity, greatly enhances Tfh cell generation. Thus, Ascl2 critically and directly initiates Tfh cell development. Decide gene expression patterns of CD4+ T cells with overexpressed Ascl2 or Tfh cells

2014-01-01 | E-GEOD-52838 | biostudies-arrayexpress

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-26 | E-GEOD-41174 | biostudies-arrayexpress