Expression data of wild type and miR-155 knockout bone marrow derived dendritic cells treated with lipopolysaccharide (LPS)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE23641 | GEO | 2010/08/16
SECONDARY ACCESSION(S): PRJNA130951
REPOSITORIES: GEO
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Project description:We used microarrays to look at overall gene expression differences between miR-155-/- and WT dendritic cells under inflammatory conditions. Bone marrow from either wild type or miR-155-/- C57Bl/6 mice was differentiated into dendritic cells by incubating with GM-CSF. These cells were then stimulated with LPS, and gene expression was performed.
2010-08-16 | E-GEOD-23641 | biostudies-arrayexpress
Project description:In response to inflammatory stimulation, dendritic cells (DCs) have a remarkable pattern of differentiation (maturation) that exhibits specific mechanisms to control immunity. Here, we show that in response to Lipopolysaccharides (LPS), several microRNAs (miRNAs) are regulated in human monocyte-derived dendritic cells. Among these miRNAs, miR-155 is highly up-regulated during maturation. Using LNA silencing combined to microarray technology, we have identified the Toll-like receptor / interleukin-1 (TLR/IL-1) inflammatory pathway as a general target of miR-155. We further demonstrate that miR-155 directly controls the level of important signal transduction molecules. Our observations suggest, therefore, that in mature human DCs, miR-155 is part of a negative feedback loop, which down-modulates inflammatory cytokine production in response to microbial stimuli.
2009-03-04 | GSE13296 | GEO
Project description:In response to inflammatory stimulation, dendritic cells (DCs) have a remarkable pattern of differentiation (maturation) that exhibits specific mechanisms to control immunity. Here, we show that in response to Lipopolysaccharides (LPS), several microRNAs (miRNAs) are regulated in human monocyte-derived dendritic cells. Among these miRNAs, miR-155 is highly up-regulated during maturation. Using LNA silencing combined to microarray technology, we have identified the Toll-like receptor / interleukin-1 (TLR/IL-1) inflammatory pathway as a general target of miR-155. We further demonstrate that miR-155 directly controls the level of important signal transduction molecules. Our observations suggest, therefore, that in mature human DCs, miR-155 is part of a negative feedback loop, which down-modulates inflammatory cytokine production in response to microbial stimuli. We devised a strategy to functionally inhibit the mature form of miR-155 with the aim of identifying the signaling pathways controlled by miR-155 during DC maturation. A LNA-modified oligonucleotide, specifically designed for miR-155 knockdown (anti-miR-155 LNA) was introduced in moDCs by nucleofection prior LPS stimulation. 24h after transfection, a reduction in miR-155 levels of 8- and 32-fold was observed by qPCR in immature and mature moDCs respectively. A comparative microarray analysis (Affymetrix U133 2.0 chip) was performed among miR-155 silenced (anti-miR-155 LNA) and control transfected (scramble LNA) moDCs, exposed or not to LPS. Thus, four samples were totally analyzed. As expected from the limited expression of miR-155 in non-activated DCs, little variation in mRNA expression (177 probe sets differentially expressed employing a cut-off of 1.5) was detected upon miR-155 silencing. Conversely, in LPS-activated cells many mRNAs (1324 probe sets, 770 up-regulated and 554 down-regulated) were affected by miR-155 inhibition.
2009-03-04 | E-GEOD-13296 | biostudies-arrayexpress
Project description:Dendritic cells isolated from murine bone marrow were cultured for 7 days and then stimulated with 50 ng/mL LPS and 5 mM ATP. Cells derived from both wild type and microRNA-155 knock-out mice. Total RNA was isolated from the cells following stimulation.
2015-07-30 | E-MTAB-2608 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute (Ago) protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. MiRNA expression can be controlled by transcription factors and can therefore be cell type- or tissue-specific. Here we have analyzed miRNA expression profiles in murine monocyte-derived dendritic cells (DCs) and macrophages upon stimulation with LPS, LDL, eLDL and oxLDL to identify not only stimuli-specific miRNA, but also to identify a hierarchical miRNA system involving miR-155. For this, miR-155 knockout dendritic cells and macrophages were also sequenced using the same stimuli. Sequencing of murine monocyte-derived dendritic cells and macrophages (each wild type and miR-155 knock out cells) matured and stimulated, respectively, by LPS, oxLDL, eLDL or LDL.
2014-01-03 | E-GEOD-48404 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute (Ago) protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. MiRNA expression can be controlled by transcription factors and can therefore be cell type- or tissue-specific. Here we have analyzed miRNA expression profiles in murine monocyte-derived dendritic cells (DCs) and macrophages upon stimulation with LPS, LDL, eLDL and oxLDL to identify not only stimuli-specific miRNA, but also to identify a hierarchical miRNA system involving miR-155. For this, miR-155 knockout dendritic cells and macrophages were also sequenced using the same stimuli.
2014-01-03 | GSE48404 | GEO
Project description:The pro-inflammatory microRNA-155 (miR-155) is highly expressed in the serum and CNS lesions of patients with multiple sclerosis (MS). The whole-body deletion of miR-155 in mice confers resistance to a mouse model of MS, EAE, by reducing the encephalogenic potential of CNS-infiltrating Th17 T cells. However, cell intrinsic roles for miR-155 during EAE have not been formally determined. Here we utilize single-cell RNA sequencing and cell-specific conditional miR-155 knockouts to determine the importance of miR-155 expression in distinct immune cell populations. Time course single-cell sequencing revealed reductions in T cells, macrophages, and dendritic cells in whole-body miR-155 knockout mice compared with wild-type controls at day 21. Deletion of miR-155 in T cells, driven by CD4 cre, reduced disease severity similar to whole-body miR-155 knockouts. CD11c cre-driven deletion of miR-155 in dendritic cells also significantly reduced EAE disease score, with both T cell and dendritic cell-specific knockouts showing a reduction in Th17 T cell infiltration into the CNS. Although miR-155 is highly expressed in infiltrating macrophages during EAE, deletion of miR-155 using LysM cre did not affect disease severity. Taken together, these data show that while miR-155 is highly expressed in most infiltrating immune cells, miR-155 has distinct roles and requirements depending on the cell type. This provides insights into which functionally relevant cell types should be targeted by the next generation of miRNA therapeutics.
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Project description:Analyze the transcriptome pattern of miR-155 deficient BMDC in both steady-state and inflammatory conditions, in comparison to WT counterparts.
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Project description:Overexpression of miR-155 in hematological tissue leads to the onset of lymphoma, and Tet-off shutdown of this overexpression reverses the disease phenotype in mir-155LSLtTA mice. This study compares the gene expression profiles of tumors with miR-155 overexpression and withdrawal.
2015-01-30 | GSE61851 | GEO
Project description:Several studies have indicated an important role for miR-155 in the pathogenesis of B-cell lymphoma. Highly elevated levels of miR-155 were indeed observed in most B-cell lymphomas with the exception of Burkitt lymphoma (BL). However, the molecular mechanisms that underlie the oncogenic role of miR-155 in B-cell lymphoma are not well understood. To identify the miR-155 targets relevant for B-cell lymphoma, we performed RNA immunoprecipitation of Argonaute 2 in Hodgkin lymphoma (HL) cells upon miR-155 inhibition and in BL cells upon ectopic expression of miR-155. We identified 54 miR-155-specific target genes in BL cells and confirmed miR-155 targeting of DET1, NIAM, TRIM32, HOMEZ, PSIP1 and JARID2. Five of these targets are also regulated by endogenous miR-155 in HL cells. Both overexpression of miR-155 and inhibition of expression of the novel miR-155 target gene NIAM increased proliferation of BL cells. In primary B-cell lymphoma NIAM-positive cases have significant lower levels of miR-155 as compared to NIAM-negative cases, suggesting that NIAM is also regulated by miR-155 in primary B-cell lymphoma. Thus, our data indicate an oncogenic role for miR-155 in B-cell lymphoma which involves targeting the tumor suppressor NIAM.
2015-02-20 | GSE64484 | GEO