Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists
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ABSTRACT:
PROVIDER: PRJNA745959 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15103141_1.fastq.gz | Fastqsanger.gz | |||
| SRR15103141_2.fastq.gz | Fastqsanger.gz | |||
| SRR15103142_1.fastq.gz | Fastqsanger.gz | |||
| SRR15103142_2.fastq.gz | Fastqsanger.gz | |||
| SRR15103143_1.fastq.gz | Fastqsanger.gz |
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2022-03-09 | GSE179945 | GEO
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Project description:Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor highly expressed by colonic epithelial cells. It plays a key role in gut homeostasis and metabolism regulation. We previously showed that PPARgamma has a role in the action of aminosalycilates (5-ASA), one of the oldest anti-inflammatory agents used in the treatment of inflammatory bowel disease. These data have prompted us to develop novel analogues of 5-ASA with greater PPARgamma-activating properties (GED). The various PPARgamma ligands appear to have some markedly different effects, some of which can induce adverse effects. The transcriptomic profiles induced by various families of PPARgamma ligands are very poorly known and especially in intestinal epithelial cells. Hence, the objectives of the present project is to compare the gene expression profile induced by GED, 5-ASA, and pioglitazone in Caco-2 cells, in order to better understand these compounds’ modes of action, to discover potential new PPARgamma target genes in intestinal epithelial cells and to explain the efficacy difference between GED and 5-ASA.
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Project description:The nuclear receptor Peroxisome Proliferator Activated Receptor gamma (PPARgamma) is known to regulate lipid metabolism in many tissues, including macrophages. Here we report that macrophage respiration is enhanced by rosiglitazone, an activating PPARgamma ligand, in a PPARgamma dependent manner. Moreover, PPARgamma is required for macrophage respiration even in the absence of exogenous ligand. Unexpectedly, the absence of PPARgamma dramatically affects the oxidation of glutamine. Both glutamine and PPARgamma have been implicated in alternative activation (AA) of macrophages and PPARgamma was required for IL4-dependent gene expression and stimulation of macrophage respiration. Remarkably, depletion of PPARgamma phenocopied the effects of glutamine depletion on transcription. Thus, PPARgamma supports alternative activation by facilitating glutamine metabolism. Yet PPARgamma expression is itself markedly increased by IL4. Thus, PPARgamma functions at the center of a feed forward loop that is central to AA of macrophages.
2018-09-06 | GSE111104 | GEO
Project description:The nuclear receptor Peroxisome Proliferator Activated Receptor gamma (PPARgamma) is known to regulate lipid metabolism in many tissues, including macrophages. Here we report that macrophage respiration is enhanced by rosiglitazone, an activating PPARgamma ligand, in a PPARgamma dependent manner. Moreover, PPARgamma is required for macrophage respiration even in the absence of exogenous ligand. Unexpectedly, the absence of PPARgamma dramatically affects the oxidation of glutamine. Both glutamine and PPARgamma have been implicated in alternative activation (AA) of macrophages and PPARgamma was required for IL4-dependent gene expression and stimulation of macrophage respiration. Remarkably, depletion of PPARgamma phenocopied the effects of glutamine depletion on transcription. Thus, PPARgamma supports alternative activation by facilitating glutamine metabolism. Yet PPARgamma expression is itself markedly increased by IL4. Thus, PPARgamma functions at the center of a feed forward loop that is central to AA of macrophages.
2018-09-06 | GSE111103 | GEO
Project description:The nuclear receptor Peroxisome Proliferator Activated Receptor gamma (PPARgamma) is known to regulate lipid metabolism in many tissues, including macrophages. Here we report that macrophage respiration is enhanced by rosiglitazone, an activating PPARgamma ligand, in a PPARgamma dependent manner. Moreover, PPARgamma is required for macrophage respiration even in the absence of exogenous ligand. Unexpectedly, the absence of PPARgamma dramatically affects the oxidation of glutamine. Both glutamine and PPARgamma have been implicated in alternative activation (AA) of macrophages and PPARgamma was required for IL4-dependent gene expression and stimulation of macrophage respiration. Remarkably, depletion of PPARgamma phenocopied the effects of glutamine depletion on transcription. Thus, PPARgamma supports alternative activation by facilitating glutamine metabolism. Yet PPARgamma expression is itself markedly increased by IL4. Thus, PPARgamma functions at the center of a feed forward loop that is central to AA of macrophages.
2018-09-06 | GSE111102 | GEO
Project description:Background: Minimal change nephrotic syndrome (MCNS) is considered to be associated with T cell dysfunction, via unknown mechanisms. Experimental observations suggest that some humoral factors alter the permeability of glomerular filtration barrier. However, the nature of such factors remains still uncertain. Methods: Using cDNA microarrays, we performed gene expression profiling of peripheral blood mononuclear cells (PBMC) from three patients with MCNS during nephrosis and remission phases. To confirm the cDNA microarray results, we performed quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analyses in nephrosis and remission samples from 20 MCNS patients and six patients with nephrotic syndrome due to membranous nephropathy. Results: Out of 24,446 genes screened, 33 genes were up-regulated (at least 1.5-fold) in PBMC from these MCNS patients during the nephrosis phase. Up-regulated genes mainly encoded proteins involved in signal transduction and cytokine response. For further examination, we selected two genes encoding provable secretary proteins, chemokine (C-C) ligand 13 (also known as monocyte chemotactic protein-4) (CCL13) and a novel galectin-related protein (HSPC159). The results of RT-PCR showed that expressions of CCL13 and HSPC159 mRNA in nephrosis PBMC samples are higher than those in remission PBMC samples from all 20 MCNS patients examined. On the other hand, these mRNA expression patterns were variable among six patients with membranous nephropathy. Conclusions: We conclude that CCL13 and HSPC159 mRNA expressions in PBMC is up-regulated in MCNS patients during the nephrosis phase. These expression changes in PBMC might be involved in the pathophysiologic processes of MCNS. Using cDNA microarrays, we performed gene expression profiling of peripheral blood mononuclear cells (PBMC) from three patients with MCNS during nephrosis and remission phases. To confirm the cDNA microarray results, we performed quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analyses in nephrosis and remission samples from 20 MCNS patients and six patients with nephrotic syndrome due to membranous nephropathy.
2010-05-25 | E-GEOD-7349 | biostudies-arrayexpress
Project description:Glomerular transcriptome from human kidney biopsies in Neptune and ERCB. A subset of samples profiled in this analysis were also profiled in Series GSE68127, and in GSE104066. Corresponding tubulointerstitial transcriptome data is submitted under GEO ID: GSE108113. RNA from the glomerular compartment was extracted and processed for hybridization on Affymetrix ST 2.1 microarrays, annotated using Human Entrez Gene ID custom CDF version 19. This dataset is part of the TransQST collection.
2018-05-17 | E-GEOD-108109 | biostudies-arrayexpress
Project description:Background: Minimal change nephrotic syndrome (MCNS) is considered to be associated with T cell dysfunction, via unknown mechanisms. Experimental observations suggest that some humoral factors alter the permeability of glomerular filtration barrier. However, the nature of such factors remains still uncertain. Methods: Using cDNA microarrays, we performed gene expression profiling of peripheral blood mononuclear cells (PBMC) from three patients with MCNS during nephrosis and remission phases. To confirm the cDNA microarray results, we performed quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analyses in nephrosis and remission samples from 20 MCNS patients and six patients with nephrotic syndrome due to membranous nephropathy. Results: Out of 24,446 genes screened, 33 genes were up-regulated (at least 1.5-fold) in PBMC from these MCNS patients during the nephrosis phase. Up-regulated genes mainly encoded proteins involved in signal transduction and cytokine response. For further examination, we selected two genes encoding provable secretary proteins, chemokine (C-C) ligand 13 (also known as monocyte chemotactic protein-4) (CCL13) and a novel galectin-related protein (HSPC159). The results of RT-PCR showed that expressions of CCL13 and HSPC159 mRNA in nephrosis PBMC samples are higher than those in remission PBMC samples from all 20 MCNS patients examined. On the other hand, these mRNA expression patterns were variable among six patients with membranous nephropathy. Conclusions: We conclude that CCL13 and HSPC159 mRNA expressions in PBMC is up-regulated in MCNS patients during the nephrosis phase. These expression changes in PBMC might be involved in the pathophysiologic processes of MCNS. Keywords: CCL13 - cDNA microarray - gene expression profile - HSPC159 - minimal change nephrotic syndrome
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