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Cellular recruitment by podocyte-derived pro-migratory factors in assembly of the human renal filter

ABSTRACT: Cellular recruitment by podocyte-derived pro-migratory factors in assembly of the human renal filter

PROVIDER: PRJNA471814 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7175490_1.fastq.gz	Fastqsanger.gz
	SRR7175490_2.fastq.gz	Fastqsanger.gz
	SRR7175500_1.fastq.gz	Fastqsanger.gz
	SRR7175500_2.fastq.gz	Fastqsanger.gz
	SRR7175491_1.fastq.gz	Fastqsanger.gz

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Cellular recruitment by podocyte-derived pro-migratory factors in assembly of the human renal filter

Project description:Analysis of monogenic kidney disease-causing genes, and secondary pathology resulting from systemic diseases including diabetes and hypertension, highlight the importance of the kidney’s filtering system, the renal corpuscles. To elucidate the developmental processes that establish the renal corpuscle, we employed single-nucleus droplet-based sequencing to capture single nuclei from the human fetal kidney. This enabled the identification of distinct cell types of the nephron (podocytes), interstitial (mesangial cells) and vascular (glomerulus) lineages that together generate the renal corpuscles. Computational trajectory analysis identified transient gene expression in the development of these cell types, predicting early precursors or mature podocytes express FBLN2, BMP4 or NTN4, in conjunction with recruitment, differentiation, and modeling of vascular and mesangial cell types into a functional filter. In vitro studies provide evidence these factors exhibit angiogenic or mesangial recruiting and inductive properties consistent with a key organizing role for podocyte precursors in kidney development. Together these studies define a spatiotemporal developmental program for the primary filtration unit of the human kidney and provide novel insights into cell interactions regulating co-assembly of constituent cell types.

2019-10-03 | GSE114569 | GEO

Cellular Recruitment by Podocyte-Derived Pro-migratory Factors in Assembly of the Human Renal Filter.

Project description:Analysis of kidney disease-causing genes and pathology resulting from systemic diseases highlight the importance of the kidney's filtering system, the renal corpuscles. To elucidate the developmental processes that establish the renal corpuscle, we performed single-nucleus droplet-based sequencing of the human fetal kidney. This enabled the identification of nephron, interstitial, and vascular cell types that together generate the renal corpuscles. Trajectory analysis identified transient developmental gene expression, predicting precursors or mature podocytes express FBLN2, BMP4, or NTN4, in conjunction with recruitment, differentiation, and modeling of vascular and mesangial cell types into a functional filter. In vitro studies provide evidence that these factors exhibit angiogenic or mesangial recruiting and inductive properties consistent with a key organizing role for podocyte precursors in kidney development. Together these studies define a spatiotemporal developmental program for the primary filtration unit of the human kidney and provide novel insights into cell interactions regulating co-assembly of constituent cell types.

| S-EPMC6817668 | biostudies-literature

Single cell transcriptomics reveal disrupted kidney filter cell-cell interactions after early and selective podocyte injury

Project description:We recently demonstrated that podocyte ablation via doxycycline-inducible deletion of an essential endogenous molecule, CTCF (iCTCFpod-/-), is sufficient to drive progressive CKD. However, the earliest events connecting podocyte injury to disrupted intercellular communication within the kidney filter remain unclear. Here we performed single-cell RNA sequencing of kidney tissue from iCTCFpod-/- mice after one week of doxycycline induction to generate a map of the earliest transcriptional effects of podocyte injury on cell-cell interactions at single cell resolution

2021-05-09 | GSE174102 | GEO

Murine Podocyte Membrane Proteomics

Project description:Podocytes are essential cells of the renal blood filter. They structurally compose the renal blood filter by interdigitating with neighboring podocytes by the means of a modified adherens junction, the slit membrane. In podocyte injury, loss of podocytes is a common feature. Podocyte loss could be mediated by the cleavage of podocyte cell adhesion molecules through the A Disintegrin and Metalloproteinase 10 (ADAM10). Here we show that ADAM10 is highly abundant at the site of blood filtration, namely at podocyte foot processes. Podocyte-expressed ADAM10 is not required for the development of the renal filter but plays a major role in podocyte injury. Following antibody-mediated injury, ADAM10 is upregulated in humans and mice. ADAM10 activity results in the cleavage of cell-cell adhesion molecules. This cleavage paves the way for an activation of the injury related Wnt/-catenin signaling pathway and for podocyte loss. We therefore conclude that ADAM10-mediated ectodomain shedding of injury-related cadherins drives podocyte injury. As part of this project, we have analyzed the membrane proteome of murin podocytes to evaluate the abundance of membrane bound proteases.

2021-02-19 | PXD022213 | Pride

Human podocyte differentiation

Project description:Microarray analysis of the molecular phenotype of the glomerular podocyte during temperature shift-induced differentiation Keywords = glomerular podocyte Keywords = differentiation

2010-05-26 | E-GEOD-1545 | biostudies-arrayexpress

Single cell transcriptomics reveal disrupted kidney filter cell-cell interactions after early and selective podocyte injury

Project description:Single cell transcriptomics reveal disrupted kidney filter cell-cell interactions after early and selective podocyte injury

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Barcode17 filter 16SrRNA

Project description:Barcode17 filter 16SrRNA

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Podocyte-specific deletion of tubular sclerosis complex 2 causes focal segmental glomerular sclerosis and progressive renal failure

Project description:Obesity can initiate and accelerate the progression of kidney diseases. However, it remains unclear how obesity affects renal dysfunction. Here, we show that a newly generated podocyte-specific tubular sclerosis complex 2 (Tsc2) knockout mouse model (Tsc2∆podocyte) develops proteinuria and dies due to end-stage renal dysfunction by 10 weeks of age. Tsc2∆podocyte mice exhibit an increased glomerular size and focal segmental glomerulosclerosis, including podocyte foot process effacement, mesangial sclerosis and proteinaceous casts. Podocytes isolated from Tsc2∆podocyte mice show nuclear factor, erythroid derived 2, like 2-mediated increased oxidative stress response on microarray analysis and their autophagic activity is lowered through the mammalian target of rapamycin (mTOR)—unc-51-like kinase 1 pathway. Rapamycin attenuated podocyte dysfunction and extends survival in Tsc2∆podocyte mice. Additionally, mTOR complex 1 (mTORC1) activity is increased in podocytes of renal biopsy specimens obtained from obese patients with chronic kidney disease. Our work shows that mTORC1 hyperactivation in podocytes leads to severe renal dysfunction and that inhibition of mTORC1 activity in podocytes could be a key therapeutic target for obesity-related kidney diseases.

2020-03-21 | GSE106828 | GEO

Human podocyte differentiation

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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.

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

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