GEO series

PUS7-Mediated Pseudouridylation of TGFBI Drives Vascular Remodeling in Pulmonary Hypertension [BID-seq]

GSE335339 Homo sapiens (human) RNA-seq (gene expression) 20 samples Submitted 2026/07/07 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 20 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: 20 samples: 20 samples, each with a distinct title — no replicated groupsGroups 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)

Background: Pulmonary hypertension (PH) is a life-threatening cardiovascular disorder characterized by irreversible pulmonary vascular remodeling and poor prognosis. RNA pseudouridylation, the most evolutionarily conserved RNA epigenetic modification, and its catalytic enzyme pseudouridine synthase 7 (PUS7) remained uncharacterized in PH, representing a major gap in understanding the epigenetic pathogenesis of the disease.

Read the full summary ↓

Methods: We generated the first single-base resolution pseudouridine (Ψ) landscape in lung tissues of PH patients using bisulfite-induced deletion sequencing (BID-seq). PUS7 expression was analyzed in hypoxic pulmonary artery endothelial cells (PAECs), the lung tissues of PH patients, and Su5416-hypoxia rodent model. The functional roles of PUS7 were investigated through genetic manipulation (PUS7-deficiency cells, AAV-mediated overexpression, endothelial cell-specific knockdown, and heterozygous knockout mice) and pharmacological inhibition using NSC107512. Results: BID-seq revealed global Ψ dysregulation in the PH patient lung tissues. Among PUS family members, PUS7 was the most markedly upregulated in these tissues and in the hypoxic PAECs. Both gene knockdown and pharmacological inhibition with NSC107512 ameliorated PH, whereas AAV-mediated PUS7 overexpression exacerbated disease progression. RNA immunoprecipitation sequencing and mutagenesis studies demonstrated that PUS7 bound to and catalyzed Ψ at position 688 of Transforming Growth Factor Beta Induced Protein (TGFBI) mRNA, thereby stabilizing TGFBI and activating Phosphatidylinositol 3 Kinase (PI3K)-Protein Kinase B (AKT) signaling pathway. Furthermore, hypoxia-inducible factor 2α (HIF-2α) directly bound the PUS7 promoter, estabilishing a HIF-2α/PUS7/TGFBI/PI3K-AKT positive feedback loop that drives PH pathogenesis. Conclusions: PUS7-mediated pseudouridylation serves as a novel epigenetic driver of PH via the HIF-2α/PUS7/TGFBI/PI3K-AKT axis, positioning PUS7 as a promising therapeutic target for this devastating disease.

This dataset

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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 GSE335339_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 PRJNA1477955 and SRA study SRP709196. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

20 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 20 sample titles: 20 distinct titles with little repetition. 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

GSM9812183 Control1_Input
GSM9812184 Control1_Treat
GSM9812185 Control2_Input
GSM9812186 Control2_Treat
GSM9812187 Control3_Input
GSM9812188 Control3_Treat
GSM9812189 Control4_Input
GSM9812190 Control4_Treat
GSM9812191 PH1_Input
GSM9812192 PH1_Treat
GSM9812193 PH2_Input
GSM9812194 PH2_Treat
GSM9812195 PH3_Input
GSM9812196 PH3_Treat
GSM9812197 PH4_Input
GSM9812198 PH4_Treat
GSM9817110 Control5_Input
GSM9817111 Control5_Treat
GSM9817112 PH5_Input
GSM9817113 PH5_Treat

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GSE334780 PUS7-Mediated Pseudouridylation of TGFBI Drives Vascular Remodeling in Pulmonary Hypertension 6 samples shares tgfbi, pseudouridylation, pus7-mediated, hypertension, remodeling, pulmonary, vascular
GSE335228 PUS7-Mediated Pseudouridylation of TGFBI Drives Vascular Remodeling in Pulmonary Hypertension II 6 samples shares tgfbi, pseudouridylation, pus7-mediated, hypertension, remodeling, pulmonary, vascular
GSE228135 Deficiency of Smooth Muscle ADAR1 RNA Editing Exacerbates Vascular Remodeling and Pulmonary Hypertension 18 samples shares hypertension, remodeling, pulmonary, vascular
GSE228133 Deficiency of Smooth Muscle ADAR1 RNA Editing Exacerbates Vascular Remodeling and Pulmonary Hypertension [pul43_RNA-seq] 12 samples shares hypertension, remodeling, pulmonary, vascular
GSE228134 Deficiency of Smooth Muscle ADAR1 RNA Editing Exacerbates Vascular Remodeling and Pulmonary Hypertension [pul51_RNA-seq] 6 samples shares hypertension, remodeling, pulmonary, vascular
GSE253415 GLI1+ cells contribute to vascular remodeling in hypoxia- and cigarette smokeinduced pulmonary hypertension 4 samples shares hypertension, remodeling, pulmonary, vascular
GSE249697 Transcriptional changes of the extracellular matrix in chronic thromboembolic pulmonary hypertension governs right ventricle remodeling and recovery 135 samples shares hypertension, remodeling, pulmonary
GSE249696 Transcriptional changes of the extracellular matrix in chronic thromboembolic pulmonary hypertension governs right ventricle remodeling and recovery [ext395_rnaseq] 95 samples shares hypertension, remodeling, pulmonary

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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.