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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

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

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.

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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.

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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.

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

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

| PRJNA628872 | ENA

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

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

| PRJNA648054 | ENA

Inhibition of Rho-associated, coiled-coil-containing protein kinase 2 in murine podocytes

Project description:Focal segmental glomerulosclerosis (FSGS) is characterized by damage to podocytes, a crucial pathological feature. While several mechanisms of podocyte injury have been suggested, many questions remain unanswered. Rho-associated, coiled-coil-containing protein kinase 2 (ROCK2), a serine/threonine kinase with diverse cellular functions, appears to play a significant role. We observed activation of ROCK2 in podocytes of mice with FSGS induced by adriamycin (ADR), as well as in cultured podocytes exposed to ADR. To delve deeper, we used conditional knockout mice where the ROCK2 gene was specifically disrupted in podocytes (PR2KO). These mice showed resistance to ADR-induced albuminuria, glomerular sclerosis, and podocyte damage. Additionally, pharmacological inhibition of ROCK2 significantly improved podocyte loss and kidney sclerosis in a mouse model of FSGS by counteracting profibrotic factors. RNA sequencing of podocytes treated with a ROCK2 inhibitor confirmed ROCK2's role as a regulator of the cyclic nucleotide signaling pathway. Our findings underscore the potential of ROCK2 inhibition as a therapeutic avenue for FSGS.

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