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Gene expression profiles of human podocyte cell line treated with and without ANGPT2

ABSTRACT: Gene expression profiles of human podocyte cell line treated with and without ANGPT2

PROVIDER: PRJNA768465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16200952_1.fastq.gz	Fastqsanger.gz
	SRR16200952_2.fastq.gz	Fastqsanger.gz
	SRR16200953_1.fastq.gz	Fastqsanger.gz
	SRR16200953_2.fastq.gz	Fastqsanger.gz
	SRR16200954_1.fastq.gz	Fastqsanger.gz

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Gene expression profiles of human podocyte cell line treated with and without ANGPT2

Project description:Glomerular diseases are the leading cause of chronic kidney diseases with pathomechanisms largely unclear. It is known that ANGPT2 regulates endothelial cell homeostasis and function via TEK/TIE2 and its deregulation causes endothelial damage. We found that ANGPT2 is upregulated in glomerular diseases and wondered whether it has any effect on glomerular podocytes and mesangial cells given that they have no or low TEK expression. We treated podocytes and mesangial cells in culture with ANGPT2 and found no overt cellular changes. RNA-seq analysis showed that gene expression was altered in both podocytes and mesangial cells and that the regulated genes in the two cell types were fundamentally different. GO and KEGG analyses showed that the two groups of regulated genes were enriched in distinct processes and pathways. These results suggest that ANGPT2 exerts effects on both podocytes and mesangial cells and that increased ANGPT2 may be involved in glomerular injury by affecting podocytes and mesangial cells in addition to endothelial cells.

2022-01-10 | GSE185292 | GEO

Gene expression profiles of human mesangial cell line treated with and without ANGPT2

Project description:Gene expression profiles of human mesangial cell line treated with and without ANGPT2

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Gene expression profiles of human mesangial cell line treated with and without ANGPT2

2022-01-10 | GSE185293 | GEO

Human podocyte cell line mRNA-seq

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OASIS overexpression in murine podocyte cell line

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Glucocorticoid receptor ChIP-seq in an immortalized podocyte cell line

Project description:The identification of the glucocorticoid receptor cistrome in a conditionally immortalized human podocyte cell line developed by transfection with the temperature-sensitive SV40-T gene

2017-07-17 | E-MTAB-5238 | biostudies-arrayexpress

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

Expression data from control and Angpt2 silenced mouse melanoma cells

Project description:The functional role of tumor cell-expressed Angpt2 still remains elusive. Here, we used mouse melanoma cells which have endgeneous Angpt2 expression and invesitgated the functional role of tumor cell-derived Angpt2. Total RNA from control and Angpt2 silenced mouse melanoma cells (RET) was isolated and was further utilized for microarray analysis using Affymetrix Mouse Gene 2.0 ST array.

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OASIS overexpression in murine podocyte cell line

Project description:Podocyte injury is involved in the onset and progression of various kidney diseases. We previously demonstrated that the transcription factor, old astrocyte specifically induced substance (OASIS) in myofibroblasts, contributes to kidney fibrosis, as a novel role of OASIS in the kidneys. Importantly, we found that OASIS is also expressed in podocytes; however, the pathophysiological significance of OASIS in podocytes remains unknown. Upon lipopolysaccharide (LPS) treatment, there is an increase in OASIS in murine podocytes. Enhanced serum creatinine levels and tubular injury, but not albuminuria and podocyte injury, are attenuated upon podocyte-restricted OASIS knockout in LPS-treated mice, as well as diabetic mice. The protective effects of podocyte-specific OASIS deficiency on tubular injury are mediated by protein kinase C iota (PRKCI/PKCι), which is negatively regulated by OASIS in podocytes. Furthermore, podocyte-restricted OASIS transgenic mice show tubular injury and tubulointerstitial fibrosis, with severe albuminuria and podocyte degeneration. Finally, there is an increase in OASIS-positive podocytes in the glomeruli of patients with minimal change nephrotic syndrome and diabetic nephropathy. Taken together, OASIS in podocytes contributes to podocyte and/or tubular injury, in part through decreased PRKCI. The induction of OASIS in podocytes is a critical event for the disturbance of kidney homeostasis.

2022-06-22 | GSE206525 | 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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