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Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression

ABSTRACT: Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression

PROVIDER: PRJNA805541 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17984630_1.fastq.gz	Fastqsanger.gz
	SRR17984630_2.fastq.gz	Fastqsanger.gz
	SRR17984631_1.fastq.gz	Fastqsanger.gz
	SRR17984631_2.fastq.gz	Fastqsanger.gz
	SRR17984632_1.fastq.gz	Fastqsanger.gz

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Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression [Pkd2]

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Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression [Pkd1]

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Epigenetic silencing of PKD1 in autosomal dominant polycystic kidney disease

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Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression

Project description:We report the findings of deletion of the miR17 binding motif from Pkd1 mRNA

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Epigenetic silencing of PKD1 in autosomal dominant polycystic kidney disease

Project description:ADPKD (Autosomal dominant polycystic kidney disease) is the most common inherited disorders and is characterized by growth of numerous cysts filled with fluid in the kidneys. Ultimately, it leads to kidney failure. The mutations of PKD1 and PKD2 account for approximately 85 and 15 percent of ADPKD, respectively. However, the mechanisms related to genetic mutation of PKD1 and PKD2 are still unclear. To investigate altered gene expression levels, Affymetrix microarray was performed using the kidney tissue from normal and ADPKD patients. Total RNAs were isolated from kidney of human normal (49 years old/ male) and ADPKD patients (62 years old/ male, 67 years old/ male) using NucleoSpin® RNA Kit (MACHEREY-NAGEL) according to the manufacturer’s instructions. We used tha Affymetrix GeneChip Human Gene 1.0 ST Array. Per RNA sample, 300 ng was used as the input into the Affymetrix procedure as recommended by the manufacturer's protocol.

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PKD1 and PKD2 mRNA cis-inhibition drives polycystic kidney disease progression.

Project description:Autosomal dominant polycystic kidney disease (ADPKD), among the most common human genetic conditions and a frequent etiology of kidney failure, is primarily caused by heterozygous PKD1 mutations. Kidney cyst formation occurs when PKD1 dosage falls below a critical threshold. However, no framework exists to harness the remaining allele or reverse PKD1 decline. Here, we show that mRNAs produced by the noninactivated PKD1 allele are repressed via their 3'-UTR miR-17 binding element. Eliminating this motif (Pkd1∆17) improves mRNA stability, raises Polycystin-1 levels, and alleviates cyst growth in cellular, ex vivo, and mouse PKD models. Remarkably, Pkd2 is also inhibited via its 3'-UTR miR-17 motif, and Pkd2∆17-induced Polycystin-2 derepression retards cyst growth in Pkd1-mutant models. Moreover, acutely blocking Pkd1/2 cis-inhibition, including after cyst onset, attenuates murine PKD. Finally, modeling PKD1∆17 or PKD2∆17 alleles in patient-derived primary ADPKD cultures leads to smaller cysts, reduced proliferation, lower pCreb1 expression, and improved mitochondrial membrane potential. Thus, evading 3'-UTR cis-interference and enhancing PKD1/2 mRNA translation is a potentially mutation-agnostic ADPKD-arresting approach.

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Polycystic Kidney Disease Progression Expression Analysis

Project description:Polycystic Kidney Disease (PKD) is a genetic disease of the kidney characterized by the gradual replacement of normal kidney parenchyma by fluid-filled cysts and fibrotic tissue. Autosomal Dominant Polycystic Kidney Disease (ADPKD) is caused by mutations in the PKD1 or PKD2 gene. Here we present an RNASeq experiment designed to investigate the effect of a kidney specific and Tamoxifen inducible knockout of the Pkd1 gene in mice. The Pkd1cko mice were harvested at different time points 2-weeks, 3-weeks, 5-weeks, 10.5-weeks, 11-weeks and 15-weeks after gene inactivation.

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