Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119637 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Renal tubulointerstitial fibrosis is the pathological feature of AAN. Aristolochic acid nephropathy (AAN)was induced by a one-time intraperitoneal injection of aristolochic acid in PBS. By RNA sequencing analysis in AAN mice, we observed the significant changes of genes important in regulating cell cycle.
2022-11-10 | GSE217176 | GEO
Project description:Aristolochic acid nephropathy (AAN) is characterised by rapidly progressive tubulointerstitial nephritis culminating in end stage renal failure and urothelial malignancy. microRNAs (miRs) are small endogenous post-transcriptional regulators of gene expression implicated in numerous physiological and pathological processes. We aimed to characterise the mechanism of AA induced cell cycle arrest and its regulation by miRs. The microarray experiment was performed to identify differentially regulated microRNAs in human proximal tubulal epithelial cells treated with aristolochic acid (AA). Analysis or differential miR expression in human proximal tubular epithelial cell line (HK-2) treated with 5ug/ml aristolochic acid, control (n=3) vs aristolochic acid (n=3)
2014-01-09 | E-GEOD-53911 | biostudies-arrayexpress
Project description:The study used a clinically relevant mouse model of chronic aristolochic acid nephropathy (AAN) to investigate the responses of proximal tubular cells during kidney fibrosis by single-nucleus RNA sequencing. The experiment involved 4 mice with AAN induced chronic renal fibrosis and 4 naive controls.
2021-06-23 | E-MTAB-9390 | biostudies-arrayexpress
Project description:Aristolochic acid nephropathy (AAN) is characterised by rapidly progressive tubulointerstitial nephritis culminating in end stage renal failure and urothelial malignancy. microRNAs (miRs) are small endogenous post-transcriptional regulators of gene expression implicated in numerous physiological and pathological processes. We aimed to characterise the mechanism of AA induced cell cycle arrest and its regulation by miRs. The microarray experiment was performed to identify differentially regulated microRNAs in human proximal tubulal epithelial cells treated with aristolochic acid (AA).
2014-01-09 | GSE53911 | 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 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: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
Project description:Aristolochic acid nephropathy induced by aristolochic acid type I in C57BL/6 mice
| PRJNA394733 | ENA
Project description:Cellular senescence is associated with the progression of chronic kidney disease (CKD), and accelerated tubular cell senescence promotes the pathogenesis of renal fibrosis. We established three animal models related to Chronic Kidney Disease, including aristolochic acid nephropathy (AAN), bilateral ischemia/reperfusion injury (BIRI) and unilateral ureter obstruction (UUO). By RNA sequencing analysis in AAN, BIRI and UUO mice, we observed significant changes of senescence and fibrosis related genes.
2024-02-03 | GSE254440 | GEO
Project description:Microarrays were used to analyse gene expression underlying early tumourigenesis in Eker rats. Distinct classes of up- and downregulated genes were identified in different preneoplasic lesion vs. microdissected normal (healthy) renal tubules. Laser capture microdissected renal basophilic atypical tubule (bAT) and basophilic atypical hyperplasia (bAH) and healthy tissue (HT) of 6-months aristolochic acid (AA)- and ochratoxin A (OTA)-treated and control (C) male Eker rats were isolated for RNA extraction and microarray analysis in order to investigate gene expression profiles induced by AA and OTA as well as to differentiate pathways specific for the bAT to bAH progression. Keywords: gene expression study, preneoplasic lesion vs. microdissected normal renal tubules
2010-02-20 | GSE10608 | GEO
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