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Gene expression in B cells from mice with the autoimmune disease nephrotoxic nephritis

ABSTRACT: Studying the differences in glycosylation in B cells of normal mice and mice with an autoimmune disease (nephrotoxic nephritis).

ORGANISM(S): Mus musculus

PROVIDER: GSE29923 | GEO | 2011/06/14

SECONDARY ACCESSION(S): PRJNA140725

REPOSITORIES: GEO

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Gene expression in B cells from mice with the autoimmune disease nephrotoxic nephritis

Project description:Studying the differences in glycosylation in B cells of normal mice and mice with an autoimmune disease (nephrotoxic nephritis). Differences in glycosylation in B cells of normal mice and mice with an autoimmune disease (nephrotoxic nephritis) were studied via gene expression analysis. RNA from mouse resting spleen B cells and B cells stimulated with antiCD40, CpG, and IL4 for 5 days, was isolated and prepared. One sample for each class was prepared. RNA was labeled and hybridized to the GLYCOv3 array. Resulting Gene expression patterns were analyzed.

2011-06-14 | E-GEOD-29923 | biostudies-arrayexpress

PGE2 promotes recovery from established Nephrotoxic Serum Nephritis in mice.

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PGE2 promotes recovery from established Nephrotoxic Serum Nephritis in mice.

Project description:We induced acute nephritis by single injection of sheep nephrotoxic serum in mice and then treated the mice with prostaglandin E2. We used microarrays to examine the global gene expressions during recovery from nephrotoxic nephritis by prostaglandin E2. Acute nephristis was induced in female mice by single injection of sheep Nephortoxc Serum (NTS), followed by prostaglandin E2 administration daily starting from day 2 after NTS administration. Mice were sacrificed on day 7 and RNAs were isolated from kidney. The RNA samples were subjected to mouse gene 1.0 ST array analysis.

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The direct effect of mycophenolate mofetil on podocytes in nephrotoxic serum nephritis

Project description:The goal of our study was to characterize glomerulus and particularly podocyte biology during MMF treatment in an immune-triggered proteinuric glomerulopathy. Therefore, nephrotoxic serum nephritis was induced in three-week old wild-type mice. On day 3, half of the mice were treated with MMF (100 mg/kgBW/d p.o.) (NTS+MMF) for one week, the other half of animals with vehicle (NTS+veh). A further group without induction and treatment served as controls (C). On day 10, we performed proteomic analysis of glomeruli.

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scRNA-seq analysis in kidney at 3 month of nephrotoxic nephritis model.

Project description:One single-cell RNA transcriptomic dataset was originated from one wild-type mouse, which was harvested at 3 months after nephrotoxic nephritis model.

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Project description:scRNA-seq analysis in kidney at 3 month of nephrotoxic nephritis model.

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Effect of Sirolimus treatment on lupus nephritis in NZB/W F1 female mice

Project description:NZB/WF1 female mice spontaneously develop autoimmune lupus nephritis. Expression profiling of kidney tissue from (a) 12 week NZB/W F1 female mice defined as asymptomatic for lupus nephritis, (b) 36 and 42 week NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 and 42 week NZB/W F1 female mice that are diseased/symptomatic for lupus nephritis and treated with Sirolimus was carried out. The goal of the study was to identify genes associated with lupus nephritis and modulated by Sirolimus, an inhibitor of mTOR. In addition, lupus nephritis genes resistant to Sirolimus therapy were also identfied This series of samples comprises of kidney tissue from (a) 12 week old NZB/W F1 female mice defined as asymptomatic for lupus nephritis (N=4), (b) 36 (N=3) and 42 week (N=3) old NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 (N=3)and 42 (N=3) week old NZB/W F1 female mice that are asymptomatic for lupus nephritis on treatment with Sirolimus

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Effect of Sirolimus treatment on lupus nephritis in NZB/W F1 female mice

2008-11-21 | GSE12024 | GEO

NEMO is distinct from IKK2 by regulating non-canonical pathway in the experimental nephrotoxic serum nephritis mouse model

Project description:Experimental nephrotoxic serum nephritis (NTN) is a model for T-cell mediated human rapid progressive glomerulonephritis. T-cell receptor (TCR) stimulation leads to intracellular signaling events ultimately causing activation of transcription factors, such as NF-κB. Using CD4creIKK2fl/fl (CD4xIKK2Δ) and CD4creNEMOfl/fl (CD4xNEMOΔ) and CD4cre mice our results demonstrated that NTN was not attenuated in CD4xIKK2Δ, CD4xNEMOΔ when compared with CD4cre mice as showing no significant kidney functional difference with respect to BUN and proteinuria data as well as histological damage. Although the percentage of CD4+ T cells infiltrating kidneys was not significantly changed between the examined groups on day 10, further analysis showed significantly reduced Tregs and significant increase in Th1 and Th17 cells in CD4xIKK2Δ and CD4xNEMOΔ mice. The expression of renal cytokines and chemokines, IL-1β, CCL2 and CCL20, was significantly changed in CD4xIKK2Δ and CD4xNEMOΔ mice when compared with nephritic CD4cre animals. The microarray data confirmed the increased expression of Th17 related cytokines in splenetic CD4+ T cells. More importantly, our array data also demonstrated the interrupted canonical pathway in nephritic CD4xNEMOΔ mice, which highlighted the possible different downstream pathway when IKK2 or NEMO is specifically deleted in lymphocytes. By combining microarray gene expression and bioinformatics analyses our data have identified genes involved in T cell proliferation and differentiation that were differentially expressed between IKK2 and NEMO deficient CD4+ T cells. We propose that better understanding the role of IKK2 and NEMO in T cell regulation will help to recognize the role of IKK2 and NEMO kinase inhibitors in the clinical application in patients with glomerulonephritis.

2018-11-30 | GSE107364 | GEO

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