Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA314844 | ENA |
REPOSITORIES: ENA
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Project description:In the present study, goal was to scan the potential biomarker for acute kidney injury induced by aristolochic acid I (AAI).We utilized the microarry analysis to investigate the microRNA (miRNA) expression profile in kidneys from rat treated by 40mg/kg AA I for 2-6 days. miRNAs with significantly different expression of global miRNA expression profile were validated by qRT-PCR. For miRNAs still significantly disregulation, we further examined the expression in plasma of rats treated with AAI dosed at 10, 20 and 40mg/kg AAI for 2-6 days by qRT-PCR. miRNAs with significantly dysregulation in plasma, their expression in brain, liver and heart was examined for kicking out the non-specific disregulation in AAI induced acute kidney injury, so that the significant dysregulation miRNAs with specificity in kidney and plasma was found as potential biomarkers for AAI induced acute kidney injury. Five control and 15 kidneys treated with 40mg/kg AAI on day 2, 4 and 6 was examined by microarray.
2016-03-10 | E-GEOD-79063 | biostudies-arrayexpress
Project description:In the present study, goal was to scan the potential biomarker for acute kidney injury induced by aristolochic acid I (AAI).We utilized the microarry analysis to investigate the microRNA (miRNA) expression profile in kidneys from rat treated by 40mg/kg AA I for 2-6 days. miRNAs with significantly different expression of global miRNA expression profile were validated by qRT-PCR. For miRNAs still significantly disregulation, we further examined the expression in plasma of rats treated with AAI dosed at 10, 20 and 40mg/kg AAI for 2-6 days by qRT-PCR. miRNAs with significantly dysregulation in plasma, their expression in brain, liver and heart was examined for kicking out the non-specific disregulation in AAI induced acute kidney injury, so that the significant dysregulation miRNAs with specificity in kidney and plasma was found as potential biomarkers for AAI induced acute kidney injury.
2016-03-10 | GSE79063 | GEO
Project description:Tissue-specific response of microRNAs to carcinogenicity and mutagenicity of aristolochic acid in rats
| PRJNA219409 | ENA
Project description:Male Sprague-Dawley rats were used to establish exhausted-exercise model by motorized rodent treadmill. Yu-Ping-Feng-San at doses of 2.18 g/kg was administrated by gavage before exercise training for 10 consecutive days. Quantitative proteomics was performed for assessing the related mechanism of Yu-Ping-Feng-San.
2022-08-12 | PXD032737 | Pride
Project description:Expression data from Aristolochic Acid and Ochratoxin A treated Tsc2 mutant (Eker) and corresponding wild type rats
| PRJNA97369 | ENA
Project description:In this study we have examined the effect of sub-cytotoxic exposure to aristolochic acids (1.65µM) at 6h, 24h and 72h on the whole-genome expression profile in a rat proximal renal tubule cell line (NRK-52E). We used microarrays to detail the mechanism of toxicity and possibly carcinogenicity of aristolochic acids in rat renal proximal cells. NRK-52E cells were cultured to confluence on 6-well plates. Cells were then exposed to aristolochic acid dissolved in DMSO (0.1%) at the IC10 concentration at 72h (1.65 ?M) or DMSO only as control. After 6h, 24h and 72h the medium was removed and RNA was extracted from the cells. Three studies were conducted at each time point.
2015-07-02 | E-GEOD-68687 | biostudies-arrayexpress
Project description:Aristolochic acid (AA) is the causative agent of urothelial tumours associated with aristolochic acid nephropathy and is also implicated in the development of Balkan endemic nephropathy-associated urothelial tumours. These tumours contain AA-characteristic TP53 mutations. We examined gene expression changes in Hupki (human TP53 knock-in) mice after treatment with aristolochic acid I (AAI) by gavage (5 mg/kg body weight). After 3, 12 and 21 days of treatment gene expression profiles were investigated using Agilent Whole Mouse 44K Genome Oligo Array. Expression profiles were significantly altered by AAI treatment in both target (kidney) and non-target (liver) tissue. Renal pathology and DNA adduct analysis confirmed kidney as the target tissue of AAI-induced toxicity. Gene ontology for functional analysis revealed that processes related to apoptosis, cell cycle, stress response, immune system, inflammatory response and kidney development were altered in kidney. Canonical pathway analysis indicated Nfkb, aryl hydrocarbon receptor, Tp53 and cell cycle signalling as the most important pathways modulated in kidney. Expression of Nfkb1 and other Nfkb-target genes was confirmed by quantitative real-time PCR (qRT-PCR) and was consistent with the induction of Nfkb1 protein. Myc oncogene, frequently over-expressed in urothelial tumours, was up-regulated by AAI on the microarrays and confirmed by qRT-PCR and protein induction. Collectively we found that microarray gene expression analysis is a useful tool to define tissue-specific responses in AAI-induced toxicity. Several genes identified such as TP53, Rb1, Mdm2, Cdkn2a and Myc are frequently affected in human urothelial cancer, and may be valuable prognostic markers in future clinical studies. Keywords: Carcinogen treatment Two-color Agilent array. A reference design was chosen that all samples were hybridised to universal mouse reference RNA (UMRR). 12-condition experiment (2 mouse organs: kidney and liver; 2 treatments: AAI and water; 3 time points: 3, 12 and 21 days). Three biological replicates for each condition. One replicate per array.
2010-06-08 | E-GEOD-18246 | biostudies-arrayexpress
Project description:MicroRNAs are small non-coding RNAs that regulate a variety of biological processes. In the last version of the miRBase database (Release 17), 720 mouse microRNAs are accompanied by only 408 rat microRNAs. Given the importance of rat as a model organism, we used next generation sequencing and microarray technologies to discover novel microRNAs in rat kidneys. Four male, 6-week-old Big Blue rats were treated with 10.0 mg/kg aristolochic acid(AA) 5 times a week for 12 weeks, four untreated rats as control. The animals were sacrificed 1 day after the last treatment and total RNA were isolated. All eight rat samples were used to deep sequencing analyses (University of Texas Southwestern Medical Center Microarray Core Facility), while 6 samples (3 AA-treated and 3 control) were used to custom vertebrate microRNA microarray analysis (LC Sciences). We used the miRanalyzer standalone version for the prediction of novel microRNAs and microRNA microarray to confirm novel microRNAs.
2011-11-02 | E-GEOD-33360 | biostudies-arrayexpress
Project description:To find out acute rejection (AR) associated microRNAs, we have employed Agilent microRNA microarray as a discovery platform to identify microRNAs with the potential to distinguish AR from controls. We first established a rat Orthotopic liver transplantation (OLT) model with AR, using Brown Norway (BN) rats that received OLT with liver grafts from Lewis rats (Lewis to BN). OLT with BN rats as the donors and recipients were also performed (BN to BN), and these rats served as the control group (non-rejection group, NR group). Then, global microRNA expression profiles of the plasma and grafts were evaluated and validated with high throughout microarray and RT-qPCR.
2020-12-26 | GSE36798 | GEO
Project description:Aristolochic acid (AA) is the causative agent of urothelial tumours associated with aristolochic acid nephropathy and is also implicated in the development of Balkan endemic nephropathy-associated urothelial tumours. These tumours contain AA-characteristic TP53 mutations. We examined gene expression changes in Hupki (human TP53 knock-in) mice after treatment with aristolochic acid I (AAI) by gavage (5 mg/kg body weight). After 3, 12 and 21 days of treatment gene expression profiles were investigated using Agilent Whole Mouse 44K Genome Oligo Array. Expression profiles were significantly altered by AAI treatment in both target (kidney) and non-target (liver) tissue. Renal pathology and DNA adduct analysis confirmed kidney as the target tissue of AAI-induced toxicity. Gene ontology for functional analysis revealed that processes related to apoptosis, cell cycle, stress response, immune system, inflammatory response and kidney development were altered in kidney. Canonical pathway analysis indicated Nfkb, aryl hydrocarbon receptor, Tp53 and cell cycle signalling as the most important pathways modulated in kidney. Expression of Nfkb1 and other Nfkb-target genes was confirmed by quantitative real-time PCR (qRT-PCR) and was consistent with the induction of Nfkb1 protein. Myc oncogene, frequently over-expressed in urothelial tumours, was up-regulated by AAI on the microarrays and confirmed by qRT-PCR and protein induction. Collectively we found that microarray gene expression analysis is a useful tool to define tissue-specific responses in AAI-induced toxicity. Several genes identified such as TP53, Rb1, Mdm2, Cdkn2a and Myc are frequently affected in human urothelial cancer, and may be valuable prognostic markers in future clinical studies. Keywords: Carcinogen treatment
2010-06-09 | GSE18246 | GEO