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Bulk RNA-seq Toxic Lipid-induced Epigenetic Activation of ICAM1 in Liver Sinusoidal Endothelium Regulates Myeloid-Driven Fibro-inflammatory Response in MASH

GSE309912 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/04/27 Platform GPL20301
At a glance

RNA-seq (gene expression) · human · 12 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
12 samples: 3 × HHSEC bulk RNA-seq - Vehicle control-veh vs 3 × HHSEC bulk RNA-seq - PA 500uM vs 3 × HHSEC bulk RNA-seq - PA 800uM vs 3 × HHSEC bulk RNA-seq - PA 500uM + LYGroups 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
Endothelial cell glycogen synthase kinase 3β promotes lipotoxic endotheliopathy and liver inflammation in MASHJCI insight · 2026
Summary (written by the submitters)
Background: Liver sinusoidal endothelial cells (LSECs) acquire a proinflammatory phenotype in metabolic dysfunction-associated steatohepatitis (MASH), characterized by elevated adhesion molecules and inflammatory mediators—a process termed lipotoxic endotheliopathy. However, the molecular drivers of this transformation remain incompletely defined.
Read the full summary ↓
Methods: We employed complementary models of lipotoxicity and MASH, including palmitate-treated primary human LSECs (in vitro), cultured precision-cut liver slices from normal human and mice liver with MASH-inducing media as well as MASH mice (ex vivo), and diet-induced MASH models (in vivo). Results: GeoMx digital spatial profiling of human MASH livers revealed enriched proinflammatory and fibrogenic signaling between LSECs and myeloid cells. Among the top upregulated genes and ligand-receptor pairs was ICAM1, whose expression correlated with disease severity and was increased in human MASH by immunostaining. ATAC-seq on primary mouse LSECs showed enhanced chromatin accessibility at the Icam1 promoter in MASH. Chromatin immunoprecipitation confirmed enrichment of the active epigenetic mark H3K27ac and BRD4 binding at the ICAM1 promoter in human LSECs under lipotoxic stress. Mechanistically, we identified the GSK3β/c-Jun/BRD4 axis as a key regulator of ICAM1 induction in LSECs. In vivo, ICAM1-neutralizing antibody or endothelial-specific epigenetic suppression reduced hepatic inflammation, injury, and fibrosis in MASH mice. Conclusion: ICAM1 is epigenetically upregulated in LSECs during lipotoxic stress and promotes myeloid cell recruitment in MASH. Targeting the epigenetic regulation of ICAM1 may offer a novel therapeutic strategy for treating human MASH.
Published in
Endothelial cell glycogen synthase kinase 3β promotes lipotoxic endotheliopathy and liver inflammation in MASH
Sano A, Guo Q, Warasnhe K et al. · JCI insight 2026 · PMID 42084928 · doi:10.1172/jci.insight.202552
This dataset
Open GSE309912 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 GSE309912_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 PRJNA1363984 and SRA study SRP644511. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42084928) ↗
Study design
3 × HHSEC bulk RNA-seq - Vehicle control-veh vs 3 × HHSEC bulk RNA-seq - PA 500uM vs 3 × HHSEC bulk RNA-seq - PA 800uM vs 3 × HHSEC bulk RNA-seq - PA 500uM + LY

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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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