Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Next Generation Sequencing of PKD2 mutant mice kidneys

ABSTRACT: This Study sought to understand the differential gene expression profile of Pkd2 mutant mice kidneys in the setting of miR-21 deletion 4 Wild type mice, 3 Pkd2 Knockout mice and 3 Pkd2-miR-21 knockout mice were analyzed

ORGANISM(S): Mus musculus

SUBMITTER: Vishal Patel

PROVIDER: E-GEOD-69556 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MicroRNA-21 Aggravates Cyst Growth in a Model of Polycystic Kidney Disease.

Lakhia Ronak R Hajarnis Sachin S Williams Darren D Aboudehen Karam K Yheskel Matanel M Xing Chao C Hatley Mark E ME Torres Vicente E VE Wallace Darren P DP Patel Vishal V

Journal of the American Society of Nephrology : JASN 20151217 8

Autosomal dominant polycystic kidney disease (ADPKD), one of the most common monogenetic disorders, is characterized by kidney failure caused by bilateral renal cyst growth. MicroRNAs (miRs) have been implicated in numerous diseases, but the role of these noncoding RNAs in ADPKD pathogenesis is still poorly defined. Here, we investigated the role of miR-21, an oncogenic miR, in kidney cyst growth. We found that transcriptional activation of miR-21 is a common feature of murine PKD. Furthermore, ...[more]

PMID: 26677864

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Project description:Purpose: MicroRNA-21 contributes to the pathogenesis of fibrogenic diseases in multiple organs including the kidney. To evaluate the therapeutic utility of antimiR-21 oligonucleotides in chronic kidney disease, we silenced miR-21 in mice that develop Alport Nephropathy due to a defect in the Col4a3 gene. The goals of this study to assess the effect of inhibiting miR-21 in the Col4a3-/- Alport Syndrome mouse model at 5.5 weeks of age. Methods: Col4a3-/-, Col4a3+/-, and Col4a3+/+ mice in the 129X1/SvJ genetic background were obtained. Mice received anti–miR-21 (25 mg/kg) or control anti-miR (25mg/kg) in phosphate-buffered saline (PBS) by inter-scapular subcutaneous injection twice per week. In some experiments mice received a range of doses from 12.5mg/kg once a week to 50mg/kg once a week. Anti–miR-21 is a high-affinity oligonucleotide complementary to the active site of miR-21. Mice received injections starting at 24 days (3.5 weeks) after birth and ending at 5, 7, 9 or 16 weeks after birth depending on the study objectives. Total RNA from kidney tissue was extracted as per manufacturerâs instructions (miREASY kit, Qiagen). RNA quality was assessed using BioAnalyzer (Agilent). mRNA expression profiles were determined using next-generation sequencing (NGS) on the Illumina HiSeq 2000 platform producing 50bp paired-end reads. Bowtie/TopHat suites were used to align the reads to mouse genome or transcriptome and RSEM were used to quantify gene abundances. Gene level counts were then normalized with the R/Bioconductor package limma using the voom/variance stabilization method. Results: Anti-miR-21 enhanced PPARÎ±/RXR activity and associated downstream signaling pathways in glomerular, tubular and interstitial cells, enhanced mitochondrial function, which reduced mitochondrial ROS production and preserved tubular cell functions. In addition, inhibition of miR-21 reduced fibrogenic and inflammatory signaling in glomerular and interstitial cells, likely as a consequence of enhanced PPARÎ±/RXR activity and mitochondrial function. Inhibition of miR-21 represents a novel therapeutic strategy for chronic kidney diseases including Alport Nephropathy. Whole kidney mRNA profiles of Col4a3+/- (triplicate) and Col4a3-/- (quadruplicates) mice treated with either PBS or antimiR-21, ending at 5.5 weeks of age, were generated by Next Generation Sequencing using Illumina HiSeq 2000

Dataset Information

Next Generation Sequencing of PKD2 mutant mice kidneys

Publications

MicroRNA-21 Aggravates Cyst Growth in a Model of Polycystic Kidney Disease.

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