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Vascular function underlies enhanced intestinal regeneration after FLASH radiation [bulk RNAseq]

GSE337790 Mus musculus (mouse) Single-cell RNA-seq 18 samples Submitted 2026/07/17 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 18 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Mus musculus (mouse)
Samples
18 samples: 7 × SIF vs 6 × SICtrol vs 5 × SICGroups 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)
Ultra-high dose-rate FLASH radiotherapy spares normal tissue while promoting tumor control, yet the basis of this protection remains unknown. Using whole-abdominal irradiation, intestinal organoids, single-cell transcriptomics, spatial vascular phenotyping, and genetic, pharmacological, and physiological perturbations, we show that the intestinal FLASH effect is the result of active heterotypic vascular-epithelial crosstalk rather than passive radiochemical protection.
Read the full summary ↓
FLASH preserves endothelial tone and perfusion along the crypt–villus axis, averting phospho-MLC–dependent vascular collapse caused by conventional irradiation. This maintains the physiological oxygen gradient and licenses early, YAP-dependent regeneration that shields transit-amplifying secretory progenitors from persistent DNA damage and drives rapid crypt reconstitution. Disrupting the oxygen gradient directly, or indirectly through endothelial VEGFR2 blockade, abolishes FLASH sparing—reinstating progenitor DNA damage, loss of DCLK1⁺ and CHGA⁺ cells, and impaired regeneration. We identify an oxygen–vasculature–YAP–progenitor axis as a central regulator of radiation-induced repair and a target to widen the therapeutic window
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 GSE337790_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1490902 and SRA study SRP715741. Searching any of these in the dataset finder brings you back here.

Study design
7 × SIF vs 6 × SICtrol vs 5 × SIC

Supports a between-group comparison across 18 samples.

How we read this: 3 replicated groups read from 18 sample titles; they account for 18 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.