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To investigate how the glycosylation of podocyte proteins changes during diabetic kidney disease

ABSTRACT: Podocytes are cells of the visceral epithelium in the kidneys and form a crucial component of the glomerular filtration barrier, contributing to size selectivity and maintaining a massive filtration surface.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32553 | GEO | 2011/10/03

SECONDARY ACCESSION(S): PRJNA147019

REPOSITORIES: GEO

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To investigate how the glycosylation of podocyte proteins changes during diabetic kidney disease

Project description:Podocytes are cells of the visceral epithelium in the kidneys and form a crucial component of the glomerular filtration barrier, contributing to size selectivity and maintaining a massive filtration surface. We are interested in pursuing a microarray analysis to identify the glycosylation-related genes that are modulated in podocytes during insulin and glucose stimulation. As such, we propose to isolate RNA from cultured AB 8/13 human podocyte cell line in their normal state and treated with different concentrations of insulin and glucose. Initially, we would like to analyze 12 samples (Normal control, 2 Starved controls, Insulin experiments 1-4, and glucose experiments 1-5). These experiments would give us information on the gene regulation changes in different healthy and diabetic conditions. In addition to providing possible identification of the unknown proteins involved with diabetic nephropathy, such analysis would provide novel information about early responses by podocytes in response to insulin and glucose level changes in vitro. The results from this analysis will be utilized to focus our research with regard to glycosylation of the proteins in the podocyte slit diaphragm.

2011-10-02 | E-GEOD-32553 | biostudies-arrayexpress

Elevation of JAML Promotes Diabetic Kidney Disease by Modulating Podocyte Lipid Metabolism

Project description:Podocytes, highly differentiated glomerular epithelial cells, are essential for the maintenance of glomerular filtration barrier. Lipid accumulation in podocytes is a major determinant of proteinuric kidney disease. By RNA-sequencing analysis, we observed the significant changes of genes important in regulating cellular lipid homeostasis in podocytes with HG treatment. We generated two mouse podocyte cell lines stably transduced with either a sh-NC lentiviral construct or a shRNA lentiviral construct designed to target JAML RNA to investigate the consequences on the gene expression profile of JAML knockdown in mouse podocytes.

2020-08-18 | GSE156367 | GEO

Localized mRNA translation mediated by Staufen is a novel mechanism regulating cytoskeletal reorganization in response to podocyte injury.

Project description:Podocyte injury that compromises the glomerular filtration barrier is an initiating feature of chronic kidney disease. Podocytes extend major cytoplasmic projections that ultimately subdivide into interdigitating foot processes to form a scaffold that supports the glomerular filtration barrier. We investigated whether podocytes, like other cell types that elaborate complex cytoplasmic projections, utilize RNA transport and local translation in order to synthesize proteins at sites distal from the cell body. Here we show that mice deficient in the RNA binding proteins Staufen1 and 2 are significantly more sensitive to podocyte injury. Furthermore, Staufen2 associates with the podocyte cytoskeleton and is present in foot processes. After injury, Staufen2 and translating ribosomes increase markedly in areas of effacement adjacent to the glomerular basement membrane. Lastly, we found that Staufen2-bound RNAs are enriched in those encoding proteins mediating cytoskeletal assembly and cell-matrix adhesion. RNA transport and localized translation is identified as a crucial process for maintaining the glomerular filtration barrier.

2022-09-01 | GSE85485 | 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

Podocyte-specific JAK2 Overexpression Worsens Diabetic Kidney Disease in Mice

Project description:Overexpression of glomerular JAK2 mRNA specifically in glomerular podocytes of 129S6 mice led to significant increases in albuminuria, mesangial expansion, glomerulosclerosis, glomerular fibronectin accumulation, and glomerular basement membrane thickening as well as a significant reduction in podocyte density in diabetic mice. Treatment with a specific JAK1/2 inhibitor partly reversed the major phenotypic changes of DKD

2017-07-31 | GSE86317 | GEO

Single glomerular podocyte RNA-seq analysis

Project description:Available single-cell RNA-seq analyses have revealed that individual cells of the same type differ substantially in gene expression. We wonder whether glomerular podocytes, the cell type that is part of glomerular filtration, also exhibit big difference in gene expression among individual cells; and what biological information could be obtained from the single-podocyte RNA-seq data. Therefore, we isolated mouse glomeruli by Dynabead/magnetic concentration method, and digested them with enzymes to dissociate the cells. We loaded the single cell suspension to a Fluidigm C1 Single-Cell Auto Prep System for single cell cDNA preparation. The cDNA samples were amplified and underwent sequecing using Illumina Highseq 2000 system.

2017-07-31 | GSE88814 | GEO

Glomerular RNA-seq data of the kidney podocyte-specific Hdac1 and Hdac2 deficient mice

Project description:Podocyte histone deacetylases (HDAC) are essential in maintaining a normal glomerular filtration barrier by modulating podocyte quiescence. Podocyte-specific loss Hdac1 and 2 in mice results in severe proteinuria and sustained DNA damage, likely caused by epigenetic alterations and deficient DNA repair, that result in podocyte senescence. Through glomeruli isolation and RNA-seq profiling from the mutant mice, we demonstrated that senescent podocytes develop a senescence-associated secretory phenotype (SASP) that contribute to the loss of podocytes. The role of HDACs in senescence may provide important clues in our understanding of how podocytes are lost following injury.

2022-10-25 | GSE216088 | GEO

Expression data for OVE26 diabetic mouse podocyte

2012-03-02 | GSE36209 | 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

Rat podocyte degradomics - N-Degradomic Analysis Reveals a Proteolytic Network Processing the Podocyte Cytoskeleton

Project description:Regulated intracellular proteolysis is essential in maintaining the integrity of podocytes and the glomerular filtration barrier of the kidney. Altered proteolytic substrate turnover has been associated with various glomerular diseases ranging from diabetic nephropathy to focal and segmental glomerulosclerosis. However, thus far it has not been possible to systematically identify proteolytically cleaved proteins although some of the proteases have been characterized. Here we applied TAILS to identify N-termini in rat glomeruli and their changes on PAN-induced injury.

2017-07-20 | PXD006356 | Pride

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