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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [RNA-seq]

ABSTRACT: We profiled total-RNA data in isolated murine podocytes during the time course of podocyte injury by ADR.

ORGANISM(S): Mus musculus

PROVIDER: GSE154955 | GEO | 2020/08/04

REPOSITORIES: GEO

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Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury [ChIP-seq]

Project description:We profiled Wt1, a key transcription factor, in purified murine podocytes based on ChIP-seq during the time course of podocyte injury by ADR.

2020-08-04 | GSE149486 | GEO

FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury

Project description:In the context of human disease, the mechanisms whereby transcription factors reprogram gene expression in reparative responses to injury are not well understood. We have studied the mechanisms of transcriptional reprogramming in disease using murine kidney podocytes as a model for tissue injury. Podocytes are a crucial component of glomeruli, the filtration units of each nephron. Podocyte injury is the initial event in many processes that lead to End Stage Kidney Disease. FOXC2 is a transcription factor known to regulate gene expression in podocytes. FOXC2 and WT1 are both required for podocyte differentiation. Using murine models and human kidney organoids, we investigated FOXC2-mediated transcriptional reprogramming during the course of podocyte injury. Correlating FOXC2 and WT1 ChIP-seq analyses demonstrated that they co-bind many genes expressed in podocytes. Reprogramming the transcriptome involved highly dynamic changes in the binding of FOXC2 and WT1 to target genes during a reparative injury response.

2023-11-01 | GSE213174 | GEO

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [WT1-MAFB_ChIP-seq]

Project description:Podocytes are highly specialized cells, but their chromatin status and the precise molecular events leading to their differentiation remain poorly defined. Here we used ChIP-Seq analysis for H3K4me3, H3K4me1 and H3K27me3 to establish the histone methylation map in adult.Loss of MafB led to the deposition of extracellular matrix, progressive foot process effacement, and kidney disease. mouse podocytes. Our data demonstrate open chromatin across podocyte specific genes and reveals that genes expressed in the mesoderm lineage become actively repressed upon podocyte differentiation. To better understand the transcriptional control of podocyte differentiation, we studied the role of transcription factor MAFB.

2024-09-30 | GSE233910 | GEO

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

Project description:Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

| PRJNA648052 | ENA

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-04 | GSE154956 | GEO

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [MAFb KO RNA-seq]

2024-09-30 | GSE233912 | GEO

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [Histons modifications ChIP-seq]

2024-09-30 | GSE233911 | GEO

Podocyte injury in Fabry nephropathy

Project description:Current therapies for Fabry disease are based on reversing intra-cellular accumulation of globotriaosylceramide (Gb3) by enzyme replacement (ERT) or chaperone mediated stabilization, thereby alleviating lysosome dysfunction. However, the therapeutic effect in the regression of end-organ damage (ie. kidney damage) is limited. Ultrastructural analysis of serial human kidney biopsies showed that long-term use of ERT reduced Gb3 accumulation in podocytes but did not alter podocyte injury. A novel CRISPR-/CAS9-mediated -Galactosidase knockout podocyte cell line confirmed ERT-mediated reversal of Gb3 accumulation without resolution of lysosomal dysfunction. Transcriptomic-based connectivity mapping and SILAC-based quantitative proteomics identified alpha-synuclein (SNCA) accumulation as a key event mediating podocyte injury.

2023-04-10 | GSE186258 | GEO

MYDGF Deficiency Exacerbates Mitotic Catastrophe of Podocytes in Glomerular Disease

Project description:Podocytes, highly differentiated glomerular epithelial cells, are essential for the maintenance of glomerular filtration barrier. Podocyte dysfunction in podocytes is a major determinant of proteinuric kidney disease. By RNA sequencing analysis in ADR-treated podocytes with or without MYDGF overexpression, we observed the significant changes of genes important in regulating cell cycle in podocytes with ADR treatment.

2021-10-06 | GSE185226 | GEO

Expression data for OVE26 diabetic mouse podocyte

Project description:Podocytes form filtration barrier through foot process around glomerualar basement membrane and selectively permit permeability of molecular smaller than albumin. Diabetes can cause podocyte pathological changes leading to high urine albumin level. Diabetic mouse model OVE26 has extremly high urine albumin and previously studies indicated its podocyte damaged. Here we try to find the key genes change in OVE26 diabetic mouse model podocyte by microarray assay while normal FVB mouse podocyte set as control. Podocyte eGFP transgenic mice were made on FVB background and crossbred to OVE26 diabetic model. Glomeruli isolated from OVE-GFP mice were digested by trypsin into signal cell. Podocytes with GFP were sorting out by FACS.

2012-03-02 | E-GEOD-36209 | biostudies-arrayexpress

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