Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA131691 | ENA |
REPOSITORIES: ENA
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Project description:Han:SPRD Cy is a spontaneous rat model of polycystic kidney disease (PKD) caused by a missense mutation in Pkdr1. Cystogenesis in this model is not clearly understood. In the current study, we performed global gene expression profiling in early-stage PKD cyst development in Cy/Cy kidneys and normal (+/+) kidneys, at 3 and 7 days of postnatal age. Expression profiles were determined by microarray analysis, followed by validation with real-time RT-PCR. Genes were selected with over 1.5 fold expression changes compared with age-matched +/+ kidneys for canonical pathway analysis. We found 9 pathways in common between 3-day and 7-day Cy/Cy kidneys. Three significantly changed pathways were designated 'VDR/RXR Activation,' 'LPS/IL-1 Mediated Inhibition of RXR Function,' and 'LXR/RXR Activation'. These results suggest that RXR mediated signaling is significantly altered in developing kidneys with mutated Pkdr1. In gene ontology analysis, the functions of these RXR-related genes were found to be involved in regulating cell proliferation and organ morphogenesis. With real-time RT-PCR analysis, the up-regulation of Ptx2, Alox15b, OSP and PCNA, major markers of cell proliferation associated with the RXR pathway, were confirmed in 3- and 7-day Cy/Cy kidneys compared with 3-day +/+ kidneys. The increased RXR protein was observed both in nuclei and cytoplasm of cystic epithelial cells in early-stage Cy/Cy kidneys, and the RXR-positive cells were strongly positive for PCNA staining. Taken together, cell proliferation and organ morphogenesis signals transduced by RXR mediated pathways may have important roles for cystogenesis in early-stage PKD in this Pkdr1-mutated Cy rat.
2011-12-09 | GSE23079 | GEO
Project description:Han:SPRD rats carry a missense mutation in Anks6 (also called Pkdr1), leading to an R823W substitution in SamCystin, a protein that contains ankyrin repeats and a sterile alpha motif (SAM). Han:SPRD Cy/+ rats develop a slowly progressing form of PKD which resembles phenotypically human ADPKD. We used microarrays to examine alterations in the renal gene expression in a rodent model of PKD, namely the Han:SPRD rat.
2015-12-02 | GSE75578 | GEO
Project description:Expression data from polycystic kidney disease susceptible and resistant rat strains
| PRJNA149463 | ENA
Project description:Polycystic kidney disease (PKD) encompasses a spectrum of inherited disorders that lead to end-stage renal disease (ESRD). There is no cure for PKD and current treatment options are limited to renal replacement therapy and transplantation. A better understanding of the pathobiology of PKD is needed for the development of new, less invasive treatments. The Lewis Polycystic Kidney (LPK) rat phenotype has been characterized and classified as a model of nephronophthisis (NPHP9, caused by mutation of the Nek8 gene) for which polycystic kidneys are one of the main pathologic features. The aim of this study was to use a GC-MS-based untargeted metabolomics approach to determine key biochemical changes in kidney and liver tissue of the LPK rat. Tissues from 16-week old LPK (n = 10) and Lewis age- and sex-matched control animals (n = 11) were used. Principal component analysis (PCA) distinguished signal corrected metabolite profiles from Lewis and LPK rats for kidney (PC-1 77%) and liver (PC-1 46%) tissue. There were marked differences in the metabolite profiles of the kidney tissues with 122 deconvoluted features significantly different between the LPK and Lewis strains. The metabolite profiles were less marked between strains for liver samples with 30 features significantly different. Five biochemical pathways showed three or more significantly altered metabolites: transcription/translation, arginine and proline metabolism, alpha-linolenic and linoleic acid metabolism, the citric acid cycle, and the urea cycle. The results of this study validate and complement the current literature and are consistent with the understood pathobiology of PKD.
2023-01-26 | MTBLS748 | MetaboLights
Project description:Global gene expression profiling in PPAR-γ agonist-treated kidneys in an orthologous rat model of human autosomal recessive polycystic kidney disease
| PRJNA150801 | ENA
Project description:Major urinary proteins (MUP) are the major component of the urinary protein fraction in house mice (Mus spp.) and rats (Rattus spp.). The structure, polymorphism and functions of these lipocalins have been well described in the western European house mouse (Mus musculus domesticus), clarifying their role in semiochemical communication. The complexity of these roles in the mouse raises the question of similar functions in other rodents, including the Norway rat, Rattus norvegicus. Norway rats express MUPs in urine but information about specific MUP isoform sequences and functions is limited. In this study, we present a detailed molecular characterization of the MUP proteoforms expressed in the urine of two laboratory strains, Wistar Han and Brown Norway, and wild caught animals, using a combination of manual gene annotation, intact protein mass spectrometry and bottom-up mass spectrometry-based proteomic approaches. Detailed sequencing of the urinary MUP isoforms reveals a less complex pattern of primary sequence polymorphism in the rat than the mouse. However, rat MUPs exhibit added complexity in the form of post-translational modifications, including the phosphorylation of Ser4 in some isoforms, and exoproteolytic trimming of specific isoforms.
2019-08-01 | PXD013986 | Pride
Project description:Gender has strong impact on kidney performance. Female gender tends to be renal protective. PKD/Mhm is rat model for human polycystic kidney disease (PKD) caused by a mutation in gene Anks6. PKD progresses faster in male rats compared with females. We used microarrays to detect gender-dependent gene expression in kidney of 36d old PKD/Mhm rats. Keywords: gender, genotype
2009-09-30 | GSE13065 | GEO
Project description:Expression data from the kidney tissue of Han:SPRD rats
| PRJNA304622 | ENA
Project description:To understand the molecular and cellular mechanisms of pathogenesis of autosomal recessive polycystic kidney disease , we performed a microarray gene expression profiling in early stage kidneys of B6C3Fe a/a-bpck mutant and wild-type mice at postnatal day 3. Genes with over 1.5-fold expression changes in mutant kidneys compared with age matched wild-type tissues were selected for analysis. This study represents the first widespread profiling of B6C3Fe a/a-bpck mutant mouse kidney and provides a valuable platform for better understanding the molecular mechanisms of polycystic kidney disease in human.
2011-12-01 | GSE34051 | GEO