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Hepatic HuR protects against atherosclerosis through bile acid production

GSE326269 Homo sapiens (human) RNA-seq (gene expression) 38 samples Submitted 2026/05/31 Platform GPL24247Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 38 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
38 samples: 12 × HM-CT vs 12 × HM-LM vs 6 × PH-WT vs 6 × PH-cKOGroups 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.
Summary (written by the submitters)
Hepatocyte-specific HuR knockout mice exhibit a lean MAFLD (metabolic-associated fatty liver disease)-like phenotype in response to high-fat diet. However, if this phenotype further impacts the development of atherosclerosis (AS) remains to be studied. Here, we report that HuR represses the production of chenodeoxycholic acid (CDCA) and taurocholic acid (TCA) in the liver through repressing the expression of CYP7A1, the rate-limiting enzyme for the central pathway of BA production.
Read the full summary ↓
HuR destabilizes Cyp7a1 mRNA by associating with its 3’UTR. In response to high-cholesterol diet (HCD), hepatic HuR increases the expression of CYP7A1 in the liver, thereby increasing the levels of CDCA and TCA in the liver and serum, activating HuR-PSPF (platelet-secreted pro-inflammatory factors) regulatory process, and aggravating HCD-induced AS in APOE (-/-) mice. Administration of TCA and CDCA activates HuR-PSPF regulatory process and at the same time aggravates HCD-induced AS. Platelet HuR ablation mitigates the effect of hepatic HuR ablation in aggravating HCD-induced AS. In the liver tissues from patients with lean MAFLD, the reduction of HuR expression, the induction of CYP7A1 expression and the activation of HuR-PFPF regulatory process, are concurrently observed. Our findings suggest an important role of hepatic HuR-CYP7A1 regulatory process in the development of AS in lean MAFLD-like lipid dysregulation.
This dataset
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.

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 GSE326269_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1445032 and SRA study SRP687630. Searching any of these in the dataset finder brings you back here.

Study design
12 × HM-CT vs 12 × HM-LM vs 6 × PH-WT vs 6 × PH-cKO

Supports a between-group comparison across 36 samples.

How we read this: 4 replicated groups read from 38 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
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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.