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Evaluation of toxicological mechanisms of ochratoxin-A in human primary proximal tubule epithelial cells

GSE289962 Homo sapiens (human) RNA-seq (gene expression) 36 samples Submitted 2025/12/10 Platform GPL34281Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 36 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
36 samples: 12 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Pervasive food contaminant ochratoxin-A induces energy crisis: Mitochondrial dysfunction in human primary proximal tubule cellsToxicology reports · 2025
Summary (written by the submitters)
Ochratoxin-A (OTA) is a fungal mycotoxin that is one of the most common food contaminants, ubiquitously found in a variety of foodstuffs worldwide. As a known nephrotoxin, hepatotoxin, and class II-b carcinogen, exposure to this compound is a major health concern. Specifically, OTA has been implicated as a potential agent in chronic kidney disease of unknown etiology (CKDu), an endemic form of chronic kidney disease that disproportionally affects rural agricultural communities and is thought to arise from environmental factors rather than diabetes and hypertension.
Read the full summary ↓
A key pathological difference between CKDu and CKD is the degeneration of the kidney proximal tubule, where OTA has been shown to accumulate. The mechanism of OTA toxicity in the human kidney remains elusive, and this study aims to elucidate OTA-induced molecular toxicological pathways using primary human proximal tubule epithelial cells (PTECs). We demonstrated that the previously reported downregulation of NRF2 target antioxidant response elements is not due to a direct interaction between NRF2 and its cytosolic binder, KEAP1, evidenced by the lack of recovery of mRNA transcripts with co-administration of NRF2 agonists, sulforaphane or tert-butylhydroquinone. Furthermore, exposure to OTA (10 uM) induces 7192 differentially expressed genes, including key regulators of mitochondrial fission and fusion. This was confirmed at the cellular level by confocal microscopy, where a breakdown of the mitochondrial network was observed at 100 nM OTA. Furthermore, OTA was found to significantly induce reactive oxygen species (mROS) and inhibit basal mitochondrial oxidative phosphorylation as well as glycolysis through measurements of oxygen consumption rate and extracellular acidification, corroborating transcriptional findings that OTA induces hypoxic response elements. In conclusion, in this work we demonstrate that OTA causes mitochondrial dysfunction and reduced ATP production, leading to a senescent-like state in PTECs characteristic of renal disease progression. These findings provide insight into early toxicological endpoints induced by OTA which have been established as pathophysiological changes involved in chronic kidney disease.
Published in
Pervasive food contaminant ochratoxin-A induces energy crisis: Mitochondrial dysfunction in human primary proximal tubule cells
Mahadeo A, Bammler TK, MacDonald J et al. · Toxicology reports 2025 · PMID 41341619 · doi:10.1016/j.toxrep.2025.102169
This dataset
Open GSE289962 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE289962_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1225654 and SRA study SRP564973. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41341619) ↗
Study design
12 conditions, mostly in triplicate
PT10_Control ×3 PT10_10uM_OTA ×3 PT10_20uM_SFN2 ×3 PT10_10uM_OTA+20uM_SFN2 ×3 PT10_5uM_tBHQ ×3 PT10_10uM_OTA+5uM_tBHQ ×3 PT6_Control ×3 PT6_10uM_OTA ×3 +4 more

Supports a between-group comparison across 36 samples.

How we read this: 12 replicated groups read from 36 sample titles; they account for 36 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

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