Similar Datasets
Project description:Analysis of the transcriptome pattern of splenic B lymphocytes after malaria infection in WT and miR-155 KO mice.
2022-01-01 | GSE69188 | 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:We used microarrays to investigate the global changes of gene expression in B cells of mir-155 Knockout mice. Analysis of mir-155 knockout cultured and activated B Cells versus wild-type cultured and activated B Cells, by microarray profiling
2013-12-03 | E-GEOD-52940 | biostudies-arrayexpress
Project description:We used microarrays to investigate the global changes of gene expression in B cells of mir-155 Knockout mice.
2013-12-03 | GSE52940 | 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.
2009-03-04 | GSE13296 | GEO
Project description:Analyze the transcriptome pattern of miR-155 deficient BMDC in both steady-state and inflammatory conditions, in comparison to WT counterparts.
2022-01-01 | GSE40027 | GEO
Project description:Analysis of the transcriptome pattern of miR-155 deficient Bone marrow-derived macrophages (BMMΦ) in both steady-state and inflammatory conditions after 6-, 12- and 24 h, in comparison to their WT counterparts.
2022-01-01 | GSE40029 | GEO
Project description:Differential gene expression profile of Tfh and non-Tfh cells from both Wt and miR-155-/- mice spleens.
2014-12-09 | GSE58371 | GEO
Project description:Differential gene expression profile of Tfh and non-Tfh cells from both Wt and miR-155-/- mice spleens. Wt and miR-155-/- mice were immunized with OVA. 8 days post immunization, CD4+CXCR+PD1+ Tfh cells and CD4+CXCR5-PD1- non Tfh cells were sorted from mice spleens for analyses.
2014-12-09 | E-GEOD-58371 | biostudies-arrayexpress
Project description:Classically activated (M1) macrophages protect from infection but can cause inflammatory disease and tissue damage while alternatively activated (M2) macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. The inflammation-associated miRNA, miR-155, was rapidly up-regulated over 100-fold in M1, but not M2, macrophages. Inflammatory M1 genes and proteins iNOS, IL-1b and TNF-a were reduced up to 72% in miR-155 knockout mouse macrophages, but miR-155 deficiency did not affect expression of genes associated with M2 macrophages (e.g., Arginase-1). Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed iNOS and TNF-a gene expression in wild-type M1 macrophages. Comparative transcriptional profiling of unactivated (M0) and M1 macrophages derived from wild-type and miR-155 knockout (KO) mice revealed an M1 signature of approximately 1300 genes, half of which were dependent on miR-155. Real-Time PCR of independent datasets validated miR-155's contribution to induction of iNOS, IL-1b, TNF-a, IL-6 and IL-12, as well as suppression of miR-155 targets Inpp5d, Tspan14, Ptprj and Mafb. Overall, these data indicate that miR-155 plays an essential role in driving the differentiation and effector potential of inflammatory M1 macrophages.
2016-07-15 | GSE77425 | GEO