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Transcriptional analysis of the impact of BMPR2 loss and BMP9 treatment on pulmonary artery endothelial cells

GSE244597 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/09/03 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: 3 × HPAECs, siControl, NS, N vs 3 × HPAECs, siControl, BMP9, N vs 3 × HPAECs, siBMPR2, NS, N vs 3 × HPAECs, siBMPR2, BMP9, NGroups 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
Circular RNA Profiling Identifies circ5078 as a BMPR2-Derived Regulator of Endothelial Proliferation and Stress ResponsesArteriosclerosis, thrombosis, and vascular biology · 2025
Summary (written by the submitters)
Pulmonary arterial hypertension (PAH) is a disease of the pulmonary endothelium associated with mutations in BMPR2, the gene encoding the bone morphogenetic protein (BMP) type II receptor (BMPR-II). Loss of BMPR-II in the pulmonary endothelium has been shown to alter the functional response of the endothelium to BMP9 treatment from growth suppression in healthy cells, to hyperproliferation with the loss of BMPR-II.
Read the full summary ↓
To investigate the molecular mechanisms underlying this phenotypic switch, we performed RNA sequencing on total RNA isolated from primary human pulmonary artery endothelial cells treated with or without BMP9 following BMPR2 knockdown or control.
Published in
Circular RNA Profiling Identifies circ5078 as a BMPR2-Derived Regulator of Endothelial Proliferation and Stress Responses
VandenBroek MM, Sharp MC, Thompson P et al. · Arteriosclerosis, thrombosis, and vascular biology 2025 · PMID 40772817 · doi:10.1161/ATVBAHA.124.322455
This dataset
Open GSE244597 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 GSE244597_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 PRJNA1023846 and SRA study SRP464449. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40772817) ↗
Study design
3 × HPAECs, siControl, NS, N vs 3 × HPAECs, siControl, BMP9, N vs 3 × HPAECs, siBMPR2, NS, N vs 3 × HPAECs, siBMPR2, BMP9, N

Supports a between-group comparison across 12 samples.

How we read this: 4 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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