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TL;DR
The study used human endothelial cells and mice to show that excess sFlt-1 causes a physical collapse of the endothelial glycocalyx, which in turn increases the stickiness of the endothelium for monocytes.
International Journal of Molecular Sciences · 9 authors, 1 centre
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The study used human endothelial cells and mice to show that excess sFlt-1 causes a physical collapse of the endothelial glycocalyx, which in turn increases the stickiness of the endothelium for monocytes.
This preclinical study investigated the mechanism by which excess soluble fms-like tyrosine kinase-1 (sFlt-1) damages the endothelial glycocalyx (eGC). Using primary human umbilical vein endothelial cells (HUVECs) in vitro, researchers demonstrated that sFlt-1 exposure decreased eGC height and increased stiffness, creating a 'collapsed' conformation without loss of glycocalyx components. This conformational change functionally increased endothelial adhesiveness to THP-1 monocytes by approximately 35%. The effects were blocked by heparin but not by vascular endothelial growth factor (VEGF). In vivo administration of sFlt-1 in mice produced similar eGC collapse in isolated aorta. The study concludes that excess sFlt-1 causes eGC collapse, favoring leukocyte adhesion and providing a novel mechanism for sFlt-1-induced endothelial dysfunction. Limitations include the static in vitro conditions and the potential confounding influence of endothelial cortex stiffness changes.