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Transcriptomic changes in Human Umbilical Vein Endothelial Cells (HUVEC) after exposure to Tumor Necrosis Factor-Alpha(TNF-a), AdipoRon, and Sphingosine Kinase Inhibitor (SKI-I)

GSE275227 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/08/01 Platform GPL24676
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 conditions, mostly in duplicateGroups 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)
Endothelial dysfunction is one of the earliest manifestations of atherosclerosis development. Adiponectin, a hormone secreted by adipose tissue with insulin-sensitizing and anti-inflammatory properties, offers protection against atherosclerosis. The pleiotropic effects of adiponectin are thought to be mediated by the ceramidase activity of adiponectin receptors.
Read the full summary ↓
Adiponectin has been shown to reduce ceramide levels in endothelial cells. Still, the effects of adiponectin on other sphingolipids and endothelial lipid metabolism are not completely elucidated. This study investigated the metabolic and sphingolipid alterations in endothelial cells linked to the protective effects of adiponectin against endothelial dysfunction. Human Umbilical Endothelial Cells (HUVECs) were treated with Tumor Necrosis Factor-alpha (TNF-α) to induce endothelial dysfunction. AdipoRon and SKI-I were used to study the effects of adiponectin and sphingosine kinase inhibition in HUVECs. Metabolic changes and sphingolipid alterations were assessed to understand changes in lipid metabolism, and RNA sequencing was used to quantify the transcriptomics changes.
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 GSE275227_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 PRJNA1149837 and SRA study SRP527400. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
control ×2 tnf ×2 adiporon ×2 ski ×2 tnf_adiporon ×2 tnf_ski ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 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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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.