RSPO3 impairs barrier function of human vascular endothelial monolayers and synergizes with pro-inflammatory IL-1

Molecular Medicine
Tom SkariaGabriele Schoedon

Abstract

Endothelial barrier dysfunction characterized by hyperpermeability of the vascular endothelium is a key factor in the pathogenesis of chronic inflammatory diseases and affects clinical outcomes. In states of chronic inflammation, mediators secreted by activated immune cells or vascular endothelium may affect the barrier function and permeability of the vascular endothelium. The matricellular R-spondin family member RSPO3 is produced by inflammatory-activated human monocytes and vascular endothelial cells, but its effects in the regulation of vascular endothelial barrier function remains elusive. The present study investigates the effects of RSPO3 on the barrier function of adult human primary macro- and micro- vascular endothelial monolayers. Tight monolayers of primary endothelial cells from human coronary and pulmonary arteries, and cardiac, brain, and dermal microvascular beds were treated with RSPO3 either alone or in combination with pro-inflammatory mediator IL-1β. Endothelial barrier function was assessed non-invasively in real-time using Electric Cell-substrate Impedance Sensing. RSPO3 treatment critically affected barrier function by enhancing the permeability of all vascular endothelial monolayers investigated. To con...Continue Reading

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Citations

Jul 12, 2019·Frontiers in Immunology·Erin Fahey, Sarah L Doyle
Jun 26, 2021·Thrombosis and Haemostasis·Gabrielle J PenningsLeonard Kritharides

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Software Mentioned

ECIS
AxioVision
GraphPad
GraphPad Prism

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