Genome-wide chromatin accessibility profiling of primary human glomerular and kidney cortex tubular outgrowth cultures (Dnase-Seq)
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PROVIDER: PRJNA476591 | ENA |
REPOSITORIES: ENA
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Project description:Genome-wide gene expression profiling of primary human glomerular and kidney cortex tubular outgrowth cultures (RNA-seq)
| PRJNA476596 | ENA
Project description:Genome-wide chromatin accessibility profiling of primary human glomerular and kidney cortex tubular outgrowth cultures For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2018-06-21 | GSE115883 | GEO
Project description:Genome-wide chromatin accessibility profiling of primary human glomerular and kidney cortex tubular outgrowth cultures For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2018-06-21 | GSE115881 | GEO
Project description:We generated primary cultures from mechanically isolated kidney glomeruli (filtration unit of the nephron) which are composed of podocytes and mesangial cells. In parallel, we generated primary kidney cortex tubule cell cultures, which are composed primarily of proximal tubule cells. Early passage cultures of these two cell types were subjected to chromatin accessibility profiling (DNase-seq) and gene expression profiling (RNA-seq). We found thousands of dynamically regulated enhancers in both cell types that potentially regulate nearby and distal target genes that are differentially expressed. These data will be useful for understanding the epigenomic regulation of gene transcription in key kidney cell types.
2018-06-19 | GSE115959 | GEO
Project description:We generated primary cultures from mechanically isolated kidney glomeruli (filtration unit of the nephron) which are composed of podocytes and mesangial cells. In parallel, we generated primary kidney cortex tubule cell cultures, which are composed primarily of proximal tubule cells. Early passage cultures of these two cell types were subjected to chromatin accessibility profiling (DNase-seq) and gene expression profiling (RNA-seq). We found thousands of dynamically regulated enhancers in both cell types that potentially regulate nearby and distal target genes that are differentially expressed. These data will be useful for understanding the epigenomic regulation of gene transcription in key kidney cell types.
2018-06-19 | GSE115960 | GEO
Project description:Glomerular-tubular crosstalk within the kidney has been proposed, but the paracrine signals enabling this remain largely unknown. The cold-shock protein Y-box binding protein 1 (YBX1) is known to regulate inflammation and kidney diseases but its role in podocytes remains undetermined. Therefore, we analyzed mice with podocyte specific Ybx1 deletion (Ybx1ΔPod). Albuminuria was increased in unchallenged Ybx1ΔPod mice, which surprisingly was associated with reduced glomerular, but enhanced tubular damage. Tubular toll-like receptor 4 (TLR4) expression, node-like receptor protein 3 (NLRP3) inflammasome activation and kidney inflammatory cell infiltrates were all increased in Ybx1ΔPod mice. In vitro, extracellular YBX1 inhibited NLRP3 inflammasome activation in tubular cells. Co-immunoprecipitation, immunohistochemical analyses, microscale cell-free thermophoresis assays, and blunting of the YBX1-mediated TLR4-inhibition by a unique YBX1-derived decapeptide suggests a direct interaction of YBX1 and TLR4. Since YBX1 can be secreted upon post-translational acetylation, we hypothesized that YBX1 secreted from podocytes can inhibit TLR4 signaling in tubular cells. Indeed, mice expressing a non-secreted YBX1 variant specifically in podocytes (Ybx1PodK2A mice) phenocopied Ybx1ΔPod mice, demonstrating a tubular-protective effect of YBX1 secreted from podocytes. Lipopolysaccharide-induced tubular injury was aggravated in Ybx1ΔPod and Ybx1PodK2A mice, indicating a pathophysiological relevance of this glomerular-tubular crosstalk. Thus, our data show that YBX1 is physiologically secreted from podocytes, thereby negatively modulating sterile inflammation in the tubular compartment, apparently by binding to and inhibiting tubular TLR4 signaling. Hence, we have uncovered an YBX1-dependent molecular mechanism of glomerular-tubular crosstalk.
2023-07-27 | GSE239313 | GEO
Project description:Multipotent progenitor cells (MPs) have been observed in human kidneys and particularly in Bowman's capsule and proximal tubules. The kidney owns the ability to repair local damage and renal MPs may play a role in the regenerative processes. Microarray technology was applied to identify differentially expressed genes among resident MPs isolated from glomeruli and tubules of normal renal tissue, renal proximal tubular epithelial cells (RPTECs) and mesenchymal stem cells (MSCs). The results of our analysis represent a starting point for further functional studies. Experiment Overall Design: This study includes three renal tissue samples which were processed to obtain 3 glomerular progenitor populations and 3 tubular ones. Three subcoltures of MSCs and RPTECs were included as well. The differences in gene expression patterns of the 4 cell types were found out.
2009-11-09 | E-GEOD-8611 | biostudies-arrayexpress
Project description:Genome-wide chromatin accessibility profiling of primary human glomerular and kidney cortex tubular outgrowth cultures For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2018-06-21 | GSE115882 | GEO
Project description:C-peptide exerts beneficial effects on glomerular hyperfiltration in type I diabetic patients. As C-peptide localizes to the nucleus, we investigated the transcriptional activities of C-peptide in proximal tubular cells isolated from diabetic rats. Two groups of proximal tubular cells isolated from type I diabetic rats: 1 treated with C-peptide, and 1 untreated. 2-3 replicates per group.
2011-07-26 | E-GEOD-24687 | biostudies-arrayexpress
Project description:Proteinuria is a cardinal feature of glomerular diseases and an important risk factor for tubulo-interstitial damage, progressive decline in kidney function, and cardiovascular complications, but the precise effects of proteinuria on tubules were previously unclear. Here, using an established mouse model of glomerulopathy, single cell sequencing, in vivo imaging and other complementary methods, we investigate in detail the spatiotemporal landscape of genetic responses to increased protein filtration along the nephron. We show that proteinuria is a potent modulator of cell signaling in tubules, and triggers extensive genetic reprogramming in distal segments, with activation of numerous developmental pathways, and a generalized convergence and loss of differentiation markers. Meanwhile, in the proximal tubule - where filtered proteins are normally endocytosed and degraded - we find that encroachment of protein uptake from early (S1) into later (S2) segments causes substantial remodeling of the latter, with dramatic downregulation of canonical processes such as organic anion/uremic toxin secretion and lipid metabolism, and a concomitant increase in reabsorptive markers. Thus, we demonstrate that the tubular effects of proteinuria are extensive, pleotropic and segment specific. Moreover, we identify protein exposure as an important environmental cue that shapes the axial topography of the nephron. Taken together, these findings could explain some well recognized phenomena in humans with chronic kidney disease (CKD).
2024-05-06 | GSE218376 | GEO