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Bone morphogenetic protein 4 (BMP4) mediates inflammation and endothelial-mesenchymal transition (EndoMT) in the vascular remodeling of angiotensin (Ang) II -induced abdominal aortic aneurysm

GSE231306 Mus musculus (mouse) Single-cell RNA-seq 2 samples Submitted 2024/07/01 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 2 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
2 samples
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)
Abdominal aortic aneurysm (AAA) is one of the most common fatal macrovascular diseases worldwide which generates huge economic burdens on humanity. Regretfully, the pathogenesis of AAA is still not well clarified. In our study, 10×single-cell sequencing revealed that endothelial cells (ECs) dysfunction and endothelial-mesenchymal transition (EndoMT) appeared in progress of angiotensin (Ang)-II induced AAA.
Read the full summary ↓
Three different types of ECs, including Mature ECs, EndoMT ECs and Injury & inflammation ECs successively appeared during the progression of AAA. Compared with Mature ECs, EndoMT ECs and Injury & inflammation ECs had stronger extracellular matrix synthesis function and lower metabolic level. Transcription factor analysis revealed that interferon regulatory factor 6 (Irf6) and homeobox A9 (Hoxa9) may be the critical regulons in Injury & inflammation ECs. According pseudotime trajectory and KEGG enrichment analysis, we speculated bone morphogenetic protein 4 (BMP4) regulated EndoMT, thus participating in Ang II-induced AAA. Our study represented BMP4 promotes phenotypic transition, cell migration and invasion of ECs by PI3K/AKT/mTOR pathways in vitro. Protein-protein interaction (PPI) analysis and co-immunoprecipitation (Co-IP) revealed that biglycan (BGN), a kind of small leucine-rich proteoglycan, directly combined with BMP4, which enhanced conversion degree of EndoMT. BMP4 reprogrammed ECs from anti-inflammatory to proinflammatory phenotype, which eventually led to AAA.
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 GSE231306_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 PRJNA963184 and SRA study SRP435164. Searching any of these in the dataset finder brings you back here.

Samples in this study

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