GEO series

Targeting calcium signaling with synthetic EB3 inhibitor promotes lung repair through FOXM1 pathway

GSE282723 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2025/10/16 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 15 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: 15 samples: 5 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.
Paper: Therapeutic targeting of endothelial calcium signaling accelerates the resolution of lung injurySignal transduction and targeted therapy · 2025

Summary (written by the submitters)

Acute respiratory distress syndrome (ARDS) is a severe pulmonary disease characterized by acute, noncardiogenic pulmonary edema and hypoxemia leading to respiratory failure with a diverse array of etiologies, including the recent SARS-CoV-2 infection. The current standard of care for ARDS remains predominantly supportive, underscoring the urgent need for targeted pharmacological interventions.

Read the full summary ↓

To address this critical gap, we have developed an inhibitor to the microtubule accessory factor end binding protein 3 (EB3), a key mediator in the pathogenesis of ARDS. During injury, EB3 in endothelial cells facilitates the cluster of inositol 1,4,5-trisphosphate receptor 3 (IP3R3) clustering on the endoplasmic reticulum surface activating pathological calcium signaling. Building on our prior research, we have designed and optimized an EB3 inhibitor, termed Vascular Therapeutics (VT)-109, with enhanced physicochemical properties using NMR approaches. Recognizing the diverse etiologies of ARDS, we evaluated the therapeutic potential of VT-109 using a range of preclinical models, including PAR-1 agonist-, endotoxin-, polymicrobial sepsis-, mechanical ventilation-, SARS-CoV-2-induced models of ARDS in mice. Treatment of VT-109 protects the lungs of mice from vascular leakage caused by ARDS by upregulating VE-cadherin at the endothelial junctions. Molecularly, VT-109 reduces the inflammatory NFAT and NFκB pathways while simultaneously activating the endothelial regenerative FOXM1 pathway. Additionally, VT-109 mitigated ARDS-induced lung injury, reduced inflammatory cytokine production, decreased morbidity and mortality, and improved lung functions. Collectively, these data demonstrate that targeting EB3-mediated pathological calcium signaling within pulmonary endothelial cells with VT-109 could provide a promising therapeutic strategy for the treatment of ARDS.

Published in

Therapeutic targeting of endothelial calcium signaling accelerates the resolution of lung injury

Chan WC, Kwok ML, Qu X et al. · Signal transduction and targeted therapy 2025 · PMID 41253746 · doi:10.1038/s41392-025-02461-y

This dataset

Open GSE282723 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 GSE282723_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 PRJNA1190072 and SRA study SRP547232. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41253746) ↗

Study design

5 conditions, mostly in triplicate

UT ×3 LPS_cont_D3 ×3 LPS_109_D3 ×3 LPS_cont_D5 ×3 LPS_109_D5 ×3

Supports a between-group comparison across 15 samples.

How we read this: 5 replicated groups read from 15 sample titles; they account for 15 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

GSM8649328 UT.1 UT
GSM8649329 UT.2 UT
GSM8649330 UT.3 UT
GSM8649331 LPS_cont_D3.1 LPS_cont_D3
GSM8649332 LPS_cont_D3.2 LPS_cont_D3
GSM8649333 LPS_cont_D3.3 LPS_cont_D3
GSM8649334 LPS_109_D3.1 LPS_109_D3
GSM8649335 LPS_109_D3.2 LPS_109_D3
GSM8649336 LPS_109_D3.3 LPS_109_D3
GSM8649337 LPS_cont_D5.1 LPS_cont_D5
GSM8649338 LPS_cont_D5.2 LPS_cont_D5
GSM8649339 LPS_cont_D5.3 LPS_cont_D5
GSM8649340 LPS_109_D5.1 LPS_109_D5
GSM8649341 LPS_109_D5.2 LPS_109_D5
GSM8649342 LPS_109_D5.3 LPS_109_D5

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