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An atypical atherogenic chemokine that promotes advanced athero¬sclerosis and hepatic lipogenesis

GSE287230 Mus musculus (mouse) RNA-seq (gene expression) 28 samples Submitted 2025/03/13 Platform GPL30172Platform GPL32159
At a glance

RNA-seq (gene expression) · mouse · 28 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
Mus musculus (mouse)
Samples
28 samples: 7 × Apoe-/-, 12 weeks HFD, WT vs 7 × Mif-2-/- Apoe-/-, 12 weeks HFD, DKOGroups 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
An atypical atherogenic chemokine that promotes advanced atherosclerosis and hepatic lipogenesisNature communications · 2025
Summary (written by the submitters)
Atherosclerosis is the underlying cause of myocardial infarction and ischemic stroke. It is a lipid-triggered inflammatory condition of arterial vessels driven by cytokines and chemokines. Chemokines that affect both vascular and metabolic pathologies are rare. Here we show that D-dopachrome tautomerase (D-DT)/macrophage migration inhibitory factor-2 (MIF-2), a paralog of the atherogenic cytokine MIF, is a novel atypical chemokine promoting athero-sclerotic plaque formation and hepatic lipid accumulation.
Read the full summary ↓
Mif-2 deficiency and its pharma-cological blockade in hyperlipidemic atherogenic Apoe-/- mice protected against lesion formation and vascular inflammation in early and advanced atherogenesis. MIF-2 promoted monocyte migration and arrest on aortic endothelial monolayers, promoted B-cell recruitment, and increased foam cell formation. Employing biochemical and cellular assays, we identified CXCR4 as a novel receptor for MIF-2. Notably, Mif-2-/-Apoe-/- mice exhibited decreased plasma lipid levels, smaller livers, and reduced hepatic lipid accumulation compared to Apoe-/- mice. Comparison of the hepatic transcriptome and lipidome between Apoe-/- and Mif-2-/-Apoe-/- mice revealed a notable enrichment of lipogenesis-related pathways, triacylglycerides, diacylglycerides, and cholesterol esters in Mif-2-proficient mice. Mechanistic experiments in hepatocytes suggested that MIF-2 regulates activation of SREBP transcription factors to induce down¬stream lipogenic genes, while upstream, this pathway was mediated by the receptors CD74 and CXCR4, and PI3K/AKT but not AMPK signaling. Proximity ligation and FLIM-FRET multiphoton-microscopy indicated that CXCR4 and CD74 form a MIF-2-inducible heteromeric complex. Lastly, MIF-2 was found upregulated in unstable human carotid plaques from atherosclerotic patients undergoing carotid endarterectomy (CEA), suggesting a role for MIF-2 in advanced stages of athero¬sclerosis. Moreover, plasma concentrations of MIF-2 were increased in patients with coronary artery disease (CAD) and correlated with disease severity. Together, these data identify MIF-2 as a novel atherogenic chemokine and CXCR4 ligand associated with CAD that not only promotes lesion formation and vascular inflammation, but also affects hepatic lipogenesis in a CD74/CXCR4/SREBP-mediated manner. MIF-2 may thus be a novel player in atherosclerotic and metabolic disease.
Published in
An atypical atherogenic chemokine that promotes advanced atherosclerosis and hepatic lipogenesis
El Bounkari O, Zan C, Yang B et al. · Nature communications 2025 · PMID 40055309 · doi:10.1038/s41467-025-57540-z
This dataset
Open GSE287230 in finder → Find more mouse 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 GSE287230_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 PRJNA1211655 and SRA study SRP557879. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40055309) ↗
Study design
7 × Apoe-/-, 12 weeks HFD, WT vs 7 × Mif-2-/- Apoe-/-, 12 weeks HFD, DKO

Supports a between-group comparison across 14 samples.

How we read this: 2 replicated groups read from 28 sample titles; they account for 14 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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