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Transcriptomic Profiling of the Sex-linked Biological Pathways of Severe Pulmonary Arterial Hypertension associated with Endothelial Cell Caveolin-1 Depletion and Chronic Hypoxia

GSE316502 Mus musculus (mouse) RNA-seq (gene expression) 35 samples Submitted 2026/04/27 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 35 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
35 samples: 12 conditions, mostly in triplicateGroups 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)
Pulmonary arterial hypertension (PAH) is distinguished by elevated blood pressure and vascular resistance in the arteries of the lungs. Patients with PAH demonstrate pulmonary vascular remodeling, wall thickening, and a high rate of morbidity due to right heart failure. Notably, while female patients are more likely to develop PAH, male patients suffer from higher morbidity rates after diagnosis.
Read the full summary ↓
The molecular mechanism(s) underlying PAH development is poorly understood, though heritable PAH linked to mutations in bone morphogenic protein receptor 2 (BMPR2) and caveolin-1 (CAV1) may provide novel insights into the disease’s pathophysiology. To interrogate this dynamic, we utilized a global CAV1 knockout (CAV1-KO) mouse model (CAV1-/-) in conjunction with chronic hypoxia to induce symptoms of PAH as demonstrated by hemodynamic and ECHO cardiography recordings. Both female and male CAV1-/- mice in chronic hypoxia demonstrated elevated right ventricular systolic pressure (RVSP) of 48.49mmHg and 47.78mmHg respectively. Female knockout mice started to die earlier in hypoxic conditions (4 wks), though male mice showed greater total mortality by the end of the 8 wks of hypoxia. In addition to wildtype controls, we compared this knockout mouse to endothelial-specific CAV1 reconstituted (CAV1-RC) knockouts and found that restoration of CAV1 expression only in endothelial cells (ECs) is sufficient to ameliorate PAH symptoms, highlighting the importance of vascular CAV1 in maintaining pulmonary artery function. RNA-sequencing of the lungs revealed that CAV1-/- is associated with downregulation of biological process gene pathways involved in cilium assembly in normoxic conditions for both sexes. In hypoxic conditions, CAV1 knockout in females leads to downregulation of BMP signaling, while male hypoxic CAV1-/- led to a significant increase in muscle cell development genes. Reconstitution of CAV1 in ECs lead to upregulation of immune signaling pathways, muscle cell development, and various cell differentiation pathways in both sexes. Females showed a unique upregulation of cilia-related pathways, while males demonstrated increased BMP signaling. These data indicate that muscle cell development, angiogenesis, cilia assembly, immune response, and BMP signaling pathways undergo sex-specific transcriptional regulation during PH development that may underlie sex differences in PH patient outcome.
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 GSE316502_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 PRJNA1403017 and SRA study SRP662259. Searching any of these in the dataset finder brings you back here.

Study design
12 conditions, mostly in triplicate
Female, WT Control, Normoxia ×3 Female, WT Control, Hypoxia ×3 Male, WT Control, Hypoxia ×3 Male, WT Control, Normoxia ×3 Male, Cav1-RC, Hypoxia ×3 Female, Cav1-RC, Hypoxia ×3 Male, Cav1-RC, Normoxia ×3 Female, Cav1-KO, Hypoxia ×3 +5 more

Supports a between-group comparison across 34 samples.

How we read this: 12 replicated groups read from 35 sample titles; they account for 34 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.