MiR-let-7e in EAE-Guan
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Ben Guan
PROVIDER: E-MEXP-3594 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:C57BL/6 mice were immunized by subcutaneous injection of MOG35-55 peptide.DIM post-treatment was given at DAY 10 of the disease progression. CD4 T cells were isolated from the brain of the mice on day 15 of the MOG35-55 peptide immunization. Total RNA was extracted and subjected to microRNA high-throughput array with Affymetrix platform.
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Project description:Mice were immunized with either MOG35-55 in CFA or with CFA alone and 14 days later PLN cells were isolated and stimulated in vitro with MOG35-55 for 3 days followed by CD4+ T cell sorting. Microarray analysis of miRNA expression profiles was performed comparing sorted CD4+ T cells from MOG35-55 in CFA immunized mice to CD4+ T cells from mice immunized with CFA alone. The data are from magnetic beads sorted CD4+ T cells from peripheral lymph nodes from 5 pooled animals per data point
2011-04-22 | E-GEOD-28473 | biostudies-arrayexpress
Project description:The study assessed the efficacy of R-flurbiprofen in experimental autoimmune encephalomyelitis (EAE) models of multiple sclerosis in mice. R-flurbiprofen, also known as tarenflurbil, is the R-enantiomer of the cyclooxyygenase inhibitor S-flurbiprofen. It is ineffective in terms of cyclooxygenase inhibition and has no relevant toxicity in humans. Oral R-flurbiprofen prevented and attenuated primary progressive EAE in C57BL6/J mice and relapsing-remitting EAE in SJL mice, even if the treatment was initiated on or after the first flare of the disease. R-flurbiprofen reduced immune cell infiltration and microglia activation and inflammation in the spinal cord, brain and optic nerve and attenuated myelin destruction and EAE-evoked hyperalgesia. R-flurbiprofen treatment increased CD4+CD25+FoxP3+ regulatory T-cells, CTLA4+ inhibitory T-cells and interleukin-10, whereas the EAE-evoked upregulation of pro-inflammatory genes in the spinal cord was strongly reduced (Sentrix6 results). The effects were associated with an increase of plasma and cortical endocannabinoids but decreased spinal prostaglandins, the latter likely due to R- to S inversion. The promising results suggest potential efficacy of R-flurbiprofen in human MS. To assess effects of R-flurbiprofen on EAE evoked gene regulations in the spinal cord a genome wide expression analysis was performed using Illumina Sentrix 6 v2 BeadChips. For the microarray study female C57BL6/J mice were immunized according to a standard protocol using the Hooke KitM-bM-^DM-" MOG35-55/CFA emulsion PTX (EK-2110, Hooke Labs, St Lawrence, MA), which contains 200 M-BM-5g myelin oligodendrocyte glycoprotein (MOG) 35-55 emulsified in 200 M-BM-5l Complete FreundM-bM-^@M-^Ys Adjuvant (CFA). The emulsion was injected subcutaneously at two sites followed by two intraperitoneal (i.p.) injections of 200 ng pertussis toxin (PTX) in phosphate buffered saline (PBS), the first 1-2 h after MOG35-55, and the second 24 h after MOG35-55. Control mice received CFA without MOG35-55 (sham mice). Treatment with R-flurbiprofen or vehicle (n = 12 per group) was started 5 days after immunization and was administered continuously via the drinking water up to the end. Spinal cords were dissected out during the flare of the disease, day 16 after immunization. For microarray analysis, total RNA was extracted from homogenizedlumbar spinal cord tissue with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit. RNA quality was checked (Nanodrop ND-1000, Agilent 2100 Bioanalyzer), and subsequently biotinylated and hybridized to Mouse Sentrix-6 V2 Expression BeadChips (Illumina). Each sample consisted of pooled lumbar spinal cord tissue from 3 animals and 3 replicate samples were analyzed per group, i.e. the analysis is based on 9 mice per group. Groups were CFA-control with vehicle treatment, CFA-control with R-flurbiprofen, EAE-vehicle and EAE-R-flurbiprofen treatment. Treatment was started 5 days after immunization. For dissection, pairs were matched according to the clinical scores. QC, labeling, hybridization and raw data evaluation and normalization were done according to standard protocols at the core facilities of the Deutsche Krebsforschungszentrum, Heidelberg, Germany.
2014-08-28 | E-GEOD-60847 | biostudies-arrayexpress
Project description:We performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex. Gene expression in motor and sensory cortex enriched tissue was assessed from four healthy and six EAE female mice. Tissue was collected from mice with paraplegia or monoplegia, with contralateral hindlimb paresis (EAE day 18-21). The gene expression profiles of the EAE mice were compared to the motor or sensory cortex of healthy control mice, resulting in a list of differentially expressed genes in healthy and EAE mice.
2014-10-01 | E-GEOD-47900 | biostudies-arrayexpress
Project description:Gene expression of murine iDCs isolated from tolerized MOG35-55-infused/MOG35-55-immunized or MOG35-55-immunized mice
| PRJNA205114 | ENA
Project description:Mice were immunized with either MOG35-55 in CFA or with CFA alone and 14 days later PLN cells were isolated and stimulated in vitro with MOG35-55 for 3 days followed by CD4+ T cell sorting. Microarray analysis of miRNA expression profiles was performed comparing sorted CD4+ T cells from MOG35-55 in CFA immunized mice to CD4+ T cells from mice immunized with CFA alone.
2011-04-22 | GSE28473 | GEO
Project description:In this study we determined whole genome gene expression of murine naive CD4+ T cells, in vitro differentiated Th17 cells, and CD4+ T cells isolated from experimental autoimmune encephalitomyelitis (EAE)-affected animals either after adoptive transfer of Th17 cells or after immunization with MOG35-55-peptide. The overall goal was to identify candidate genes involved in T cell pathology, encephalitogenicity and plasticity. These findings could then be correlated to multiple sclerosis pathology. Naive CD4+ T cells were isolated from B6.2d2 transgenic mice with MOG-specific T cell receptors and differentiated in vitro into Th17 cells. These Th17 cells were adoptively transferred into lymphopenic RAG1-/- mice to induce EAE. Further, EAE was induced by immunizing wild-type C57BL/6 mice with MOG35-55 peptide. RNA was extracted from naive CD4+ T cells, Th17 cells, and from CD4+ T cells isolated from the CNS of EAE-affected mice for gene expression analysis. Replicates from three independent experiments were analyzed.
2015-02-26 | E-GEOD-57098 | biostudies-arrayexpress
Project description:Recent data from our group, demonstrate that infusion of myelin oligodendrocyte glycoprotein (MOG35-55) peptide, leads to induction of MOG35-55-specific Tregs and subsequent suppression of Experimental Autoimmune Encephalomyelitis (EAE), the mouse model of multiple sclerosis. Amelioration of EAE was accompanied by reduced MOG-specific Th1 and Th17 responses in the draining lymph nodes (dLNs). Phenotypic analysis of the dLNs of MOG-infused mice revealed a significant Treg-mediated reduction in the recruitment of 7AAD-CD3-CD19-CD11c+CD11bhighGr-1+ iDCs compared to non-infused control immunized mice. Focusing on the delineation of novel molecules/genes that are involved in the MOG-specific Treg-mediated suppression of autoimmune responses, we have isolated highly purified iDCs from MOG infused and non-infused control immunized mice.
2015-04-20 | GSE47210 | GEO
Project description:Recent data from our group, demonstrate that infusion of myelin oligodendrocyte glycoprotein (MOG35-55) peptide, leads to induction of MOG35-55-specific Tregs and subsequent suppression of Experimental Autoimmune Encephalomyelitis (EAE), the mouse model of multiple sclerosis. Amelioration of EAE was accompanied by reduced MOG-specific Th1 and Th17 responses in the draining lymph nodes (dLNs). Phenotypic analysis of the dLNs of MOG-infused mice revealed a significant Treg-mediated reduction in the recruitment of 7AAD-CD3-CD19-CD11c+CD11bhighGr-1+ iDCs compared to non-infused control immunized mice. Focusing on the delineation of novel molecules/genes that are involved in the MOG-specific Treg-mediated suppression of autoimmune responses, we have isolated highly purified iDCs from MOG infused and non-infused control immunized mice. Gene expression profiles of iDCs isolated from tolerized or immunized mice. Affymetrix MG 430 2.0 whole genome arrays were performed in triplicates for tolerized iDCs and immunized iDCs (6 arrays in total, 5 of them were analyzed). To obtain genes significantly regulated in iDCs upon tolerization with MOG35-55, the expression profiles of iDCs isolated from tolerized or immunized mice were compared to each other. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 µg cRNA hybridized to the 6 GeneChip arrays: Group1 iDCs isolated from tolerized mice, Group2 iDCs isolated from immunized mice.
2015-04-20 | E-GEOD-47210 | biostudies-arrayexpress
Project description:In this study we determined whole genome gene expression of murine naive CD4+ T cells, in vitro differentiated Th17 cells, and CD4+ T cells isolated from experimental autoimmune encephalitomyelitis (EAE)-affected animals either after adoptive transfer of Th17 cells or after immunization with MOG35-55-peptide. The overall goal was to identify candidate genes involved in T cell pathology, encephalitogenicity and plasticity. These findings could then be correlated to multiple sclerosis pathology.
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