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Related Experiment Video

Updated: Jul 27, 2025

Zinc-finger Nuclease Enhanced Gene Targeting in Human Embryonic Stem Cells

Zinc-finger Nuclease Enhanced Gene Targeting in Human Embryonic Stem Cells

Published on: August 23, 2014

Targeting EB3-IP

Man Long Kwok¹, Melissa Geyer¹, Wan Ching Chan¹

¹Department of Pharmacology and Regenerative Medicine, College of Medicine, and.

American Journal of Respiratory Cell and Molecular Biology

|June 8, 2023

Summary

This summary is machine-generated.

A new peptide, CIPRI, targets the EB3-IP3R3 interaction to reduce pulmonary vascular leakage and inflammation in acute respiratory distress syndrome (ARDS). This therapeutic strategy shows promise for treating lung injury and improving survival in sepsis models.

Keywords:

calcium signaling endotoxemia lung inflammation sepsis vascular leakage

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Last Updated: Jul 27, 2025

Zinc-finger Nuclease Enhanced Gene Targeting in Human Embryonic Stem Cells

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Published on: August 23, 2014

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Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line

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Published on: September 28, 2022

Area of Science:

Pulmonary Medicine
Molecular Biology
Pharmacology

Background:

Acute respiratory distress syndrome (ARDS) lacks targeted treatments, relying on supportive care.
Pulmonary vascular leakage and inflammation are key contributors to ARDS pathology.
End binding protein 3 (EB3) amplifies calcium signaling, increasing vascular leakage.

Purpose of the Study:

To develop a pharmacological treatment targeting EB3-IP3R3 interaction for pulmonary vascular leakage.
To investigate the therapeutic potential of a novel peptide inhibitor, CIPRI.

Main Methods:

Designed and synthesized a 14-amino acid peptide, CIPRI, to disrupt EB3-IP3R3 interaction.
Tested CIPRI in vitro using lung microvascular endothelial cells and in vivo using endotoxin-challenged mice.
Assessed calcium signaling, endothelial cell junction integrity, lung injury, vascular leakage, and inflammatory markers.

Main Results:

CIPRI disrupted EB3-IP3R3 interaction in vitro and in vivo.
CIPRI mitigated calcium release and preserved endothelial cell junctions.
CIPRI treatment reduced lung injury, vascular leakage, NFAT signaling, and pro-inflammatory cytokines, improving survival in sepsis models.

Conclusions:

Targeting the EB3-IP3R3 interaction with CIPRI is a viable strategy to combat pulmonary vascular hyperpermeability.
CIPRI demonstrates therapeutic potential for inflammatory lung diseases like ARDS and sepsis.
This approach offers a novel pharmacological avenue for critical care medicine.