Transcriptomic analysis of primary human T cells and murine RAW 264.7 macrophages 3D cultured in different collagen densities
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ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE124876 | GEO | 2019/03/01
REPOSITORIES: GEO
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Project description:Transcriptomic analysis of primary human T cells and murine RAW 264.7 macrophages 3D cultured in different collagen densities
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2016-10-22 | E-GEOD-32090 | biostudies-arrayexpress
Project description:We found that co-culturing BNL CL.2 liver cells with RAW 264.7 macrophages increased IRP binding in the first. To further investigate this modulation we investigated the gene expression profile in BNL CL.2 cells cultured alone, with iron, with RAW 264.7 macrophages or in the presence of both iron and macrophages. This novel reconstituted liver cell-macrophage communication pathway with the present gene expression data provides a platform for addressing how macrophages participate in the iron homeostasis of liver cells and, ultimately, in systemic iron homeostasis.
2016-10-22 | GSE32090 | GEO
Project description:Immunoresponsive gene 1 (IRG1) is one of the highest induced genes in macrophages under pro-inflammatory conditions and its function has been recently described: it codes for immune-responsive gene 1 protein/cis-aconitic acid decarboxylase (IRG1/CAD), an enzyme catalyzing the production of itaconic acid from cis-aconitic acid, a tricarboxylic acid (TCA) cycle intermediate. Itaconic acid possesses specific antimicrobial properties inhibiting isocitrate lyase, the first enzyme of the glyoxylate shunt, an anaplerotic pathway that bypasses the TCA cycle and enables bacteria to survive on limited carbon conditions. To elucidate the mechanisms underlying itaconic acid production through IRG1 induction in macrophages, we examined the transcriptional regulation of IRG1. Using a combination of literature information, transcription factor prediction models and genome-wide expression arrays, we inferred the regulatory network of IRG1 in mouse and human macrophages.
2016-02-25 | GSE76562 | GEO
Project description:IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine. We determined that adenosine suppressed the expression of many IFNg-regulated pro-inflammatory cytokines, chemokines, and other pro-atherogenic genes. Keywords: treatment response
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Project description:Microbiota contributes to induction of type 2 diabetes by high-fat/high-sugar (HFHS), but which organs/pathways are impacted by microbiota remains unknown. Using multi-organ network and transkingdom analyses, we found that microbiota-dependent. impairment of OXPHOS /mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germfree mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3-dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance. doi: https://doi.org/10.1084/jem.20220017
2022-05-24 | GSE203516 | GEO
Project description:IFNg is a pro-inflammatory and pro-atherogenic cytokine that leads to macrophage activation. Adenosine has well-documented anti-inflammatory properties. We used microarrays to compare the global gene expression profile in mouse macrophages stimulated with IFNg alone and those cells treated with IFNg and adenosine. We determined that adenosine suppressed the expression of many IFNg-regulated pro-inflammatory cytokines, chemokines, and other pro-atherogenic genes. Keywords: treatment response RAW 264.7 cells were treated for 4 hours with either IFNg or IFNg plus adenosine. Following treatment, total RNA was extracted and treatment groups were pooled from 2 separate experiments for hybridization of Affymetrix microarrays.
2009-12-30 | E-GEOD-14612 | biostudies-arrayexpress
Project description:Macrophages have many functions, such as acting as phagocytic pathogens, antigen presentation and playing a key role in immune response. Tripartite motif containing 59 (TRIM59) protein is highly expressed in a variety of tumor cells and regulates the proliferation of tumor cells as well as their innate immune response. Recent studies have shown that the expression of TRIM59 was differentially expressed under different stimuli of activated macrophages, however, the effects of TRIM59 on macrophage gene expression profiles are still unknown. In our study, we constructed RAW 264.7 macrophages with high and low expression of TRIM59, and used transcriptome sequencing to identify the effects of TRIM59 on macrophage gene expression profiles. Results showed that TRIM59 affected an abundant number of genes, and may affect phagocytosis and cell cycles.
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Project description:The CD20-homolog Ms4a8a was identified as a novel molecule of tumor-associated macrophages directly enhancing tumor growth. In addition, Ms4a8a is expressed in typical M2-dominated pathologies as late stage Trypanosoma congolense and Taenia crassiceps infections. For its induction a complex stimulation with pro- and antiinflammatory mediators is necessary. In this study we analysed how forced over-expression of Ms4a8a modulates the TLR4 response of RAW264.7 macrophages. We used microarrays to assess gene regulatory functions of Ms4a8a in Raw264.7 macrophages
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