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GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [Pkd2- RNAseq]

ABSTRACT: GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [Pkd2- RNAseq]

PROVIDER: PRJNA637874 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11943484_1.fastq.gz	Fastqsanger.gz
	SRR11943484_2.fastq.gz	Fastqsanger.gz
	SRR11943485_1.fastq.gz	Fastqsanger.gz
	SRR11943485_2.fastq.gz	Fastqsanger.gz
	SRR11943486_1.fastq.gz	Fastqsanger.gz

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GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [GDNF RNAseq]

Project description:GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [GDNF RNAseq]

| PRJNA637873 | ENA

GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD

Project description:GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD

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GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [Pkd2- RNAseq]

Project description:We report a profile of 35 genes that are differentially expressed in Pkd2- tubuloids compared to controls.

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Genotyping of PKD2 Arg803* in Taiwan ADPKD Cohort

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Identification of ADPKD-related Genes and Pathways in the Cells Overexpressing PKD2

Project description:Based on the dosage effect hypothesis, renal cysts could arise in transgenic murine models overexpressing either PKD1 or PKD2, which are causal genes responsible for autosomal dominant polycystic kidney disease (ADPKD). To prove whether PKD genes overexpression is a universal mechanism driving cystogenesis or is merely restricted to rodents, other animal models are required. Previously, we failed to observe any renal cysts in a PKD2 overexpression transgenic pig model partially due to epigenetic silencing of transgene. Thus, to explore the feasibility of pig models and identification potential affected genes/pathways related to ADPKD, LLC-PK1 cells with high PKD2 expression were generated. RNA-seq was performed and MYC, IER3, ADM were found to be commonly upregulated genes in different PKD2 overexpression cell models. MYC is a well-characterized factor contributing to cystogenesis, and ADM is a biomarker for chronic kidney disease. Thus, theses genes might be indicators of disease progression. Additionally, some ADPKD associated pathways, e.g., MAPK, were also enriched in the cells. Besides, GO analysis demonstrated proliferation, apoptosis, cell cycle regulation, which are hall marks of ADPKD were disturbed. Therefore, our experiment not only identified some biomarkers or indictors regarding ADPKD, but also demonstrated high PKD2 expression would like to drive cystogenesis in future porcine models.

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GDNF drives rapid tubule morphogenesis in novel 3D in vitro model for ADPKD [GDNF RNAseq]

Project description:We report a significant change in epithelial differentiation pathways and principal cell specific transcription factors in tubuloids with a GDNF pulse, when compared to control tubuloid cultures.

2020-06-08 | GSE151949 | GEO

Transcriptional profiling in adult onset ADPKD mouse model based on Pkd2 inactivation

Project description:We performed unbiased transcriptional profiling in an adult-onset Pkd2 mouse model at an early stage before cysts formed using as controls wild type and PC2+cilia double knockout mice which are protected from ADPKD. By a tripartite comparison, we identified differetially expressed genes which have significant different expression in Pkd2-only knockout with same direction of change from both wild type and Pkd2+Cilia double knockout.

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Project description:Purpose: Determine the differential gene expression pattern between wildtype, Pkd2-KO and Pkd2-miR-214 KO mice Methods: kidney mRNA profiles of Pkd2-KO and Pkd2-mir-214-KO mice was sequenced with N of 3 in each group Results: 972 differentially expressed transcripts were identified between Pkd2-KO kidneys and Pkd2-miR-214-KO kidneys Conclusion: Deletion of miR-214 promotes interstitial inflammation in mouse models of ADPKD

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GDNF drives rapid tubule morphogenesis in a novel 3D <i>in vitro</i> model for ADPKD.

Project description:Cystogenesis is a morphological consequence of numerous genetic diseases of the epithelium. In the kidney, the pathogenic mechanisms underlying the program of altered cell and tubule morphology are obscured by secondary effects of cyst expansion. Here, we developed a new 3D tubuloid system to isolate the rapid changes in protein localization and gene expression that correlate with altered cell and tubule morphology during cyst initiation. Mouse renal tubule fragments were pulsed with a cell differentiation cocktail including glial-derived neurotrophic factor (GDNF) to yield collecting duct-like tubuloid structures with appropriate polarity, primary cilia, and gene expression. Using the 3D tubuloid model with an inducible Pkd2 knockout system allowed the tracking of morphological, protein, and genetic changes during cyst formation. Within hours of inactivation of Pkd2 and loss of polycystin-2, we observed significant progression in tubuloid to cyst morphology that correlated with 35 differentially expressed genes, many related to cell junctions, matrix interactions, and cell morphology previously implicated in cystogenesis.This article has an associated First Person interview with the first author of the paper.

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Project description:Identification of ADPKD-related Genes and Pathways in the Cells Overexpressing PKD2

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