Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression in a conditionally immortalized mouse podocyte cell line

ABSTRACT: The specialized glomerular epithelial cell (podocyte) of the kidney is a complex cell that is often damaged in glomerular diseases. Study of this cell type is facilitated by an in vitro system of propagation of conditionally immortalized podocytes. Here, genes that are differentially expressed in this in vitro model of podocyte differentiation are evaluated.

ORGANISM(S): Mus musculus

PROVIDER: GSE23856 | GEO | 2010/08/28

SECONDARY ACCESSION(S): PRJNA130631

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression in a conditionally immortalized mouse podocyte cell line

Project description:The specialized glomerular epithelial cell (podocyte) of the kidney is a complex cell that is often damaged in glomerular diseases. Study of this cell type is facilitated by an in vitro system of propagation of conditionally immortalized podocytes. Here, genes that are differentially expressed in this in vitro model of podocyte differentiation are evaluated. Conditionally immortalized undifferentiated mouse podocytes were cultured under permissive conditions at 33*C. Podocytes that were differentiated at the non-permissive conditions at 37*C were used for comparison.

2010-08-28 | E-GEOD-23856 | biostudies-arrayexpress

Glomerular podocyte RNA-seq data of the podocyte-specific Profilin1 deficient mice

Project description:The progression of proteinuric kidney disease is associated with podocyte loss but the mechanisms remain unclear. Podocytes reenter the cell cycle to repair damaged ds DNA breaks. However, unsuccessful repair results in podocytes crossing the G1/S checkpoint and undergoes abortive cytokinesis. In this study, we identified Pfn1 as a major contributor in maintaining glomerular integrity and its loss in mice results in severe proteinuria, and kidney failure due to podocyte mitotic catastrophe, characterized by abundant multinucleated cells. Reentry of podocytes were identified by using FUCCI-2aR mice, accompanying the alteration of cell-cycle associated proteins, such as P21, P53, Cyclin B, and Cyclin D. Podocyte-specific translating ribosome affinity purification (TRAP) and RNAseq revealed a reduction of Ribosomal RNA-processing protein 8 (Rrp8) and re-expression of Rrp8 partially rescued the in-vitro phenotype. Clinical analysis of patients with proteinuric kidney disease demonstrated multinucleated podocytes and reduced podocyte profilin1 in kidney tissue. These results suggest that profilin is indispensible in regulating podocyte cell cycle and its disruption contributes to podocyte loss through mitotic catastrophe.

2023-12-01 | GSE227414 | 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

Human iPSC-derived glomeruli provide an advanced model to interrogate podocyte biology and accurately recapitulate podocytopathy

Project description:Podocytes are highly specialised cells within the glomeruli of the kidney that maintain the filtration barrier by forming interdigitating foot processes and slit-diaphragms. Disruption to these features result in proteinuria and glomerulosclerosis. Studies into podocyte biology and disease have previously relied on conditionally immortalised cell lines due to the non- proliferative nature of this cell type. Here we describe an advanced model to study both podocyte and glomerular biology using isolated glomeruli from kidney organoids derived from human pluripotent stem cells.

2018-12-04 | GSE111992 | GEO

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

The change of mRNA expression in murine immortalized podocyte after miR-26a silencing

Project description:The change of mRNA expression in murine immortalized podocyte were analyzed after miR-26a silencing. These results provide a basical information of molecular pathology in podocyte biology. Mouse podocytes immortalized by temperature sensitive SV40 were used. Podocyte cultures grown at 33 °C were trypsinized and then cultured with RPMI-1640 without antibiotics in 24-well plates at 60–70% confluence for 2 days. On day 3, an anti-miR negative control (40 pmol) or the miR-26a miRNA inhibitor (40 pmol) was transfected to podocytes. The cells were analyzed after culturing for 24 hour.

2014-10-01 | E-GEOD-51210 | biostudies-arrayexpress

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

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

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

Expression data for OVE26 diabetic mouse podocyte

2012-03-02 | GSE36209 | GEO