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Proximal tubular transcriptional response to aristolochic acid

ABSTRACT: Proximal tubular transcriptional response to aristolochic acid

PROVIDER: PRJNA634008 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11816618.fastq.gz	Fastqsanger.gz
	SRR11816619.fastq.gz	Fastqsanger.gz
	SRR11816620.fastq.gz	Fastqsanger.gz
	SRR11816621.fastq.gz	Fastqsanger.gz
	SRR11816622.fastq.gz	Fastqsanger.gz

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Proximal tubular transcriptional response to aristolochic acid

Project description:The proximal tubule is particularly susceptible to acute kidney injury caused by ischemic or toxic insults, due to its high oxygen demand, and role in excreting drugs such as DNA-damaging chemotherapeutics. AKI triggers PT cell de-differentiation, expression or pro-inflammatory and pro-fibrotic signaling molecules, and a dramatic shift in PT cell metabolism with severe suppression of fatty acid oxidation. The aim of this study was to investigate the transcriptional changes that occur in the S2 and S3 segments of the PT in response to the DNA damaging agent aristolochic acid I (AAI).

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Single-Nucleus RNA Sequencing Identifies New Classes of Proximal Tubular Epithelial Cells in Kidney Fibrosis

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

Loss of proximal tubular Kruppel-like factor 15 (KLF15) exacerbates kidney injury through loss of fatty acid oxidation

Project description:KLF15 has a critical role in other kidney cell types, but its role in mediating proximal tubular (PT) fatty acid oxidation (FAO) in AKI has not been determined. PT-specific KLF15 knockdown (Klf15PTKO) and control Klf15fl/fl mice were treated with multiple low doses of the PT-specific DNA-damaging agent aristolochic acid I (AAI) and RNA-sequencing of kidney cortex undertaken. Klf15PTKO exhibited worse kidney injury than Klf15fl/fl mice after AAI treatment. Immune system and integrin signaling pathways were significantly upregulated in Klf15PTKO versus Klf15fl/fl mice. Metabolic pathways, specifically FAO, were significantly downregulated in Klf15PTKO versus Klf15fl/fl mice, including PPARalpha signaling.

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Biomarkers for aristolochic acid nephrotoxicity

Project description:Biomarkers for aristolochic acid nephrotoxicity

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Aristolochic acid nephropathy induced by aristolochic acid type I in C57BL/6 mice

Project description:Aristolochic acid (AA) is a nephrotoxic carcinogen responsible for acute kidney injury, chronic renal failure, and associated urothelial cancers. This study aims to determine the genes in xenobiotic metabolism pathway regulated by AA and clarify the molecular mechanism underlying their action.

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HK2/AA Stimulation

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)

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Project description:C-peptide exerts beneficial effects on glomerular hyperfiltration in type I diabetic patients. As C-peptide localizes to the nucleus, we investigated the transcriptional activities of C-peptide in proximal tubular cells isolated from diabetic rats. Two groups of proximal tubular cells isolated from type I diabetic rats: 1 treated with C-peptide, and 1 untreated. 2-3 replicates per group.

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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.

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