Key result
Kawasaki disease sera induces endothelial hyperpermeability via NRP1 and VEGFR2 interacting with ANGPTL4 and VEGF.
Why the study?
The mechanisms involved in the development of endothelial barrier dysfunction during Kawasaki disease vasculitis are still largely unclear.
Does soluble NRP1 reduce endothelial hyperpermeability induced by Kawasaki disease sera in human coronary artery endothelial cells?
Population
Human coronary artery endothelial cells and sera from patients with Kawasaki disease and healthy controls
Comparison
Soluble NRP1 or NRP1 silencing vs bevacizumab treatment or VEGFR2 silencing
Design
Preclinical experimental study
Authors
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Soluble NRP1 may attenuate hyperpermeability from Kawasaki sera in endothelial cells; hypothesis-generating for NRP1/ANGPTL4/VEGF axis targeting.
Does soluble NRP1 reduce endothelial hyperpermeability induced by Kawasaki disease sera in human coronary artery endothelial cells?
Neutralization of hyperpermeability factors by soluble NRP1 may be a novel therapeutic strategy for Kawasaki disease vasculitis by targeting the NRP1/ANGPTL4/VEGF axis.
Huang et al. (2021) studied Kawasaki disease. Sera from patients with Kawasaki disease vs. Sera from healthy controls was evaluated on Endothelial cell permeability. Sera from Kawasaki disease patients induced endothelial cell hyperpermeability via overexpressed NRP1 and VEGFR2 interacting with increased ANGPTL4 and VEGF.