Glomerular and Tubular Transcriptome in the Cprobe Cohort
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ABSTRACT:
PROVIDER: PRJNA748043 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Glomerular Transcriptome in the Cprobe Cohort
| PRJNA748052 | ENA
Project description:Glomerular Transcriptome from subjects in the NEPTUNE cohort. A number of samples profiled in this analysis were also profiled in Series GSE68127, and Series GSE108113. RNA from the glomerular compartment of was extracted and processed for hybridization on Affymetrix microarrays. Contributor: NEPTUNE Consortium. This dataset is part of the TransQST collection.
2018-05-17 | E-GEOD-104066 | biostudies-arrayexpress
Project description:Tubular Transcriptome in the Cprobe Cohort
| PRJNA748051 | ENA
Project description:Glomerular Transcriptome from subjects in the NEPTUNE cohort. A number of samples profiled in this analysis were also profiled in Series GSE68127, and Series GSE108113.
2018-05-17 | GSE104066 | GEO
Project description:Glomerular Transcriptome from subjects in the NEPTUNE cohort
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Project description:Glomerular Transcriptome in the Neptune Cohort
2022-04-13 | GSE197307 | 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:Glomerular Transcriptome in the Nephrotic Syndrome study network cohort
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Project description:Nonsurgical rodent chronic kidney disease (CKD) models for both glomerular and tubular injuries are currently limited. This study aimed to develop a rat model of CKD by combining anti-Fx1A with N(ω)-nitrophenyl-L-arginine methyl ester (L-NAME) administration. The rats were assigned to groups receiving L-NAME, anti-Fx1A, anti-Fx1A + L-NAME, or vehicle. Renal function, stiffness, injury biomarkers, histopathology and genome-wide transcriptomic changes were evaluated. Protein and renal injury biomarker levels in the urine were elevated in the anti-Fx1A alone and combination groups. Shear wave elastography revealed increased stiffness of the kidneys in all treatment groups. Histopathological evaluation revealed glomerular injury, characterized by enlarged glomeruli with increased hyaline materials in both anti-Fx1A groups and tubular degeneration/regeneration in the renal cortex of all treated groups, with the highest incidence and severity in the combination group. These tubular changes were sometimes accompanied by interstitial mononuclear cell infiltrates and interstitial fibrosis. Proteinuria and mild changes in blood, urine renal injury biomarkers and imaging endpoints were noted in association with these histopathologic changes. The concurrence and higher incidence and/or severity of glomerular and tubular injuries in the combination group indicate that this would be a useful and relevant CKD model suitable for mechanistic, pharmacologic and toxicological investigations.
2024-12-06 | GSE283627 | 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.
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