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Enhancer and super-enhancer landscape in ADPKD

ABSTRACT: We performed ChIP-Seq on 16 day old control and Pkd1 mutant kidneys using an antibody to H3K27ac to determine the enhancer and superenhancer landscape in ADPKD

ORGANISM(S): Mus musculus

PROVIDER: GSE189153 | GEO | 2022/05/18

REPOSITORIES: GEO

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Enhancer and super-enhancer landscape in ADPKD

Project description:Enhancer and super-enhancer landscape in ADPKD. 2 biological replicates of Pkd1RC/- cells are analyzed via H3K27ac ChIP-Seq

2022-05-17 | GSE202681 | GEO

Mettl3/m6A promotes translation of pathogenic mRNAs to mediate cystogenesis in mouse models of ADPKD

Project description:Purpose: Determine the differential m6A methylation pattern of Mettl3 between wildtype, Pkd1F/RC-KO and Pkd1F/RC-Mettl3-DKO mouse kidneys. Methods: m6A RNA IP using the Magna MeRIP™ m6A Kit (EMD Millipore, catalog #17-10499) was performed on P18 wildtype, Pkd1F/RC-KO and Pkd1F/RC-Mettl3-DKO mouse kidney samples. Two biological replicate samples from each genotype were sequenced. Each sample was a pool of 6 kidneys of the same genotype. The input samples were also sequenced to obtain mRNA profiles. Results: 133 mRNAs were found to be differentially hypermethylated in the Pkd1-KO kidneys compared to the control kidneys and differentially hypomethylated in the Pkd1-Mettl3-DKO kidneys compared to the Pkd1-KO kidneys. Two key pathogenic mRNAs namely, c-Myc and Avpr2 were identified and validated as Mettl3 targets. The mRNA transcript levels were unchanged between Pkd1-KO and Pkd1-Mettl3-DKO kidneys. Conclusion: Mettl3/m6A promotes translation of pathogenic mRNAs to mediate cystogenesis in mouse models of ADPKD.

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Enhancer and super-enhancer landscape in ADPKD

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Expression data from renal cysts of autosomal dominant polycystic kidney disease (ADPKD) patients

Project description:To elucidate the molecular pathways that modulate renal cyst growth in autosomal dominant polycystic kidney disease (ADPKD) Keywords: Disease state analysis We performed global gene profiling on renal cysts of different size (small cysts: less than 1 ml, n=5; medium cysts: between 10-25 ml, n=5; large cysts: greater than 50 ml, n=3) and minimally cystic tissue (MCT, n=5) from five PKD1 polycystic kidneys. Additionally, non-cancerous renal cortical tissue from three nephrectomized kidneys with isolated renal cell carcinoma was used as normal control tissue (n=3). This dataset is part of the TransQST collection.

2009-08-14 | E-GEOD-7869 | biostudies-arrayexpress

Gene expression profiling in human ADPKD cell lines

Project description:Changes in gene expression levels were identified by microarray. Samples were human kidney epithelial cell lines derived from patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) and unaffected controls. Autosomal Dominant Polycystic Kidney Disease (ADPKD), the most common inherited kidney disease, is due to mutations in PKD1 (85%) or PKD2 (15%) but has a highly variable phenotypic disease expression. We conducted parallel microarray profiling in normal and diseased human PKD1 cystic kidney cells to identify altered signatures of microRNA and mRNA target genes potentially implicated in disease expression.

2017-07-05 | E-MTAB-4188 | biostudies-arrayexpress

MicroRNA expression profiling in human ADPKD cell lines

Project description:Changes in microRNA expression levels were identified by microarray. Samples were human kidney epithelial cell lines derived from patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) and unaffected controls. Autosomal Dominant Polycystic Kidney Disease (ADPKD), the most common inherited kidney disease, is due to mutations in PKD1 (85%) or PKD2 (15%) but has a highly variable phenotypic disease expression. We conducted parallel microarray profiling in normal and diseased human PKD1 cystic kidney cells to identify altered signatures of microRNA and mRNA target genes potentially implicated in disease expression. This dataset contains the results of the microRNA analysis.

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Project description:DNA methylation aberrancies are found in autosomal dominant polycystic kidney disease (ADPKD) which suggest the methylome to be a promising therapeutic target. However, the impact of combining DNA methylation inhibitors (DNMTi) and ADPKD drugs in treating ADPKD and on disease-associated methylation patterns has not been fully explored. To test this, ADPKD drugs, metformin and tolvaptan (MT), were delivered in combination with DNMTi 5-aza-2’-deoxycytidine (Aza) to 2D or 3D cystic Pkd1 heterozygous renal epithelial cells (PKD1-Het cells) as free drugs or within nanoparticles to enable direct delivery for future in vivo applications. We found Aza synergizes with MT to reduce cell viability and cystic growth. Reduced representation bisulfite sequencing (RRBS) was performed across 4 groups: PBS, Free-Aza (Aza), Free-Aza+MT (F-MTAza), and Nanoparticle-Aza+MT (NP-MTAza). Global methylation patterns showed that while Aza alone induces a unimodal intermediate methylation landscape, Aza+MT recovers the bimodality reminiscent of somatic methylomes. Importantly, site-specific methylation changes associated with F-MTAza and NP-MTAza were largely conserved including hypomethylation at ADPKD-associated genes. Notably, we report hypomethylation of cancer-associated genes implicated in ADPKD pathogenesis as well as new target genes that may provide additional therapeutic effects. Overall, this study motivates future work to further elucidate the regulatory mechanisms of observed drug synergy and apply these combination therapies in vivo.

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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.

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Expression patterns of key miRNAs in end-stage ADPKD kidneys

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