GEO series

RNA-seq of human atherosclerotic carotid plaque tissue from diabetic patients

GSE311535 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/12/17 Platform GPL16791

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: 6 × Carotid, Asymptomatic, Subject vs 6 × Carotid, Symptomatic, SubjectGroups 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: Insulin use promotes pro-inflammatory changes in the transcriptome of atherosclerotic plaques in patients with diabetes mellitusJournal of molecular and cellular cardiology plus · 2025

Summary (written by the submitters)

Diabetes Mellitus is associated with increased risk of myocardial infarctions and strokes due to accelerated atherosclerotic plaque development and rupture. The mechanisms driving plaque rupture in the diabetic setting remain unclear. We sequenced ribosome-depleted total RNA from carotid plaques obtained from diabetic subjects undergoing carotid endarterectomy with high-grade stenosis, who either recently experienced a carotid-related ischemic cerebrovascular event (Symptomatic, n=6) or had no such event (Asymptomatic, n=6).

Read the full summary ↓

Principal component analysis of the most variable transcripts demonstrated that sex and insulin use, rather than plaque rupture status, were the major contributors to the variability in the dataset. Hierarchical clustering further highlighted the importance of these factors in the dataset but also included two clusters whose expression was elevated in the symptomatic group. These clusters were enriched with transcripts for immunoglobulins and matrix metalloproteinases, suggesting increased B-cell infiltration and extracellular matrix degradation in the symptomatic plaques. We identified only two transcripts, RNU2-1 and PI4KAP1, as significantly up-regulated in the symptomatic group. We identified 35 transcripts with altered expression in subjects on insulin therapy, including regulators of B-cells (MZB1), T cells (BTN3A1, BTN3A2, BTN3A3, CD96, and CTSW), and macrophages (MPEG1). Next, we used spatial deconvolution to focus on differentially expressed genes in the fibrous cap of the carotid plaques. In the symptomatic group, we identified elevated levels of five angiogenesis-associated transcripts (ALS2CL, EPHB4, SMAD1, PREX2, EFNA5), suggesting increased intraplaque neovascularization in ruptured plaques. Thus, insulin use significantly impacts the transcriptome of atherosclerotic plaques, promoting vascular inflammation.

Published in

Insulin use promotes pro-inflammatory changes in the transcriptome of atherosclerotic plaques in patients with diabetes mellitus

Bradford A, Yoshida T, Sukhanov S et al. · Journal of molecular and cellular cardiology plus 2025 · PMID 41377472 · doi:10.1016/j.jmccpl.2025.100829

This dataset

Open GSE311535 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 GSE311535_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 PRJNA1368953 and SRA study SRP648262. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41377472) ↗

Study design

6 × Carotid, Asymptomatic, Subject vs 6 × Carotid, Symptomatic, Subject

Supports a between-group comparison across 12 samples.

How we read this: 2 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

GSM9326646 Carotid, Asymptomatic, Subject 1 Carotid, Asymptomatic, …
GSM9326647 Carotid, Asymptomatic, Subject 2 Carotid, Asymptomatic, …
GSM9326648 Carotid, Symptomatic, Subject 1 Carotid, Symptomatic, S…
GSM9326649 Carotid, Symptomatic, Subject 2 Carotid, Symptomatic, S…
GSM9326650 Carotid, Symptomatic, Subject 3 Carotid, Symptomatic, S…
GSM9326651 Carotid, Symptomatic, Subject 4 Carotid, Symptomatic, S…
GSM9326652 Carotid, Asymptomatic, Subject 3 Carotid, Asymptomatic, …
GSM9326653 Carotid, Symptomatic, Subject 5 Carotid, Symptomatic, S…
GSM9326654 Carotid, Symptomatic, Subject 6 Carotid, Symptomatic, S…
GSM9326655 Carotid, Asymptomatic, Subject 4 Carotid, Asymptomatic, …
GSM9326656 Carotid, Asymptomatic, Subject 5 Carotid, Asymptomatic, …
GSM9326657 Carotid, Asymptomatic, Subject 6 Carotid, Asymptomatic, …

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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.