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Effect of endothelial YAP/TAZ on neuroinflammation and outcome after ischemic stroke in mice

GSE265949 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2025/12/04 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 16 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
16 samples: 4 × brain, Mouse brain endothelial cells, YT-iKO, MCAo, vs 4 × brain, Mouse brain endothelial cells, YT-iKO, Sham, vs 4 × brain, Mouse brain endothelial cells, CTRL, MCAo, vs 4 × brain, Mouse brain endothelial cells, CTRL, Sham,Groups 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
Loss of Endothelial YAP/TAZ Reduces the Size of Chronic Stroke Lesions and Alters the Endothelial EnvironmentJournal of the American Heart Association · 2026
Summary (written by the submitters)
In the acute phase of ischemic stroke, endothelial cell (EC) dysfunction leads to breakdown of the blood-brain barrier with increased vascular permeability, vascular inflammation, and transendothelial migration of leukocytes. ECs are also critical for long-term regenerative processes, such as post-stroke angiogenesis, enabling the transition from brain injury to repair.
Read the full summary ↓
Yes-associated protein 1 (YAP) and WW domain-containing transcriptional regulator 1 (TAZ) are co-transcriptional regulators of EC proliferation and apoptosis. Several studies showed that YAP/TAZ is essential for developmental angiogenesis. However, the role of YAP/TAZ in adult angiogenesis and particularly in experimental stroke is unknown. Here, we subjected mice with an inducible EC-specific deletion of YAP and TAZ (YT-iKO) to 30-min middle cerebral artery occlusion (MCAo) followed by reperfusion to investigate the effects of endothelial YAP/TAZ on acute and long-term outcome after ischemic stroke. First, we examined mRNA expression of genes related to YAP/TAZ signaling in ischemic brain tissue, such as Id1, Smad6, Ankrd and Ccn2. We found a transient induction with highest expression levels acutely after stroke. Surprisingly, endothelial YAP/TAZ deficiency resulted in reduced lesion volumes 28 days after MCAo, whereas acute lesion size 3 days after stroke did not differ. Moreover, Yap/Taz iEC-KO animals showed no gross differences in vessels morphology 28 days after stroke, and no effect was detected on blood vessel density and EC density. We therefore speculated whether angiogenesis-independent effects of YAP/TAZ might also be associated with improved long-term outcome after stroke. To better understand the underlying mechanisms, we performed RNA sequencing of ECs isolated from ischemic brain tissue of YT-iKO compared with CTRL animals 72h post stroke. Here, we identified differently expressed gene sets involved in inflammatory responses. Therefore, we studied the non-endothelial tissue environment of the brain. We found, that EC YAP/TAZ deletion led to increased expression of anti-inflammatory genes accompanied by increased infiltration of myeloid cells, suggesting a protective phenotype. Besides, acute microglia proliferation was reduced in Y/T-iKO animals. Overall, our results provide new insights into the role of endothelial YAP/TAZ in neuroinflammation after cerebral ischemia. YAP/TAZ may therefore be a potential therapeutic target for the treatment of ischemic stroke.
Published in
Loss of Endothelial YAP/TAZ Reduces the Size of Chronic Stroke Lesions and Alters the Endothelial Environment
Göttert R, Kikhia M, Herzog ML et al. · Journal of the American Heart Association 2026 · PMID 41294142 · doi:10.1161/JAHA.124.040079
This dataset
Open GSE265949 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 GSE265949_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 PRJNA1105028 and SRA study SRP504246. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41294142) ↗
Study design
4 × brain, Mouse brain endothelial cells, YT-iKO, MCAo, vs 4 × brain, Mouse brain endothelial cells, YT-iKO, Sham, vs 4 × brain, Mouse brain endothelial cells, CTRL, MCAo, vs 4 × brain, Mouse brain endothelial cells, CTRL, Sham,

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 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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