Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 108, Issue 3, Pages 999-1011Publisher
OXFORD UNIV PRESS
DOI: 10.1002/JLB.2A0320-283RR
Keywords
atherosclerosis; EPH signaling; monocyte-endothelial interaction
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Funding
- Dutch Heart Foundation [2013T127]
- Rembrandt Institute for Cardiovascular Science
- European Research Area Network on Cardiovascular Diseases [038 MISsCVD]
- Dutch Heart Foundation (CVON RECONNECT)
- Dutch Science Organisation [016.156.445]
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The molecular basis of atherosclerosis is not fully understood and mice studies have shown that Ephrins and EPH receptors play a role in the atherosclerotic process. We set out to assess the role for monocytic EPHB2 and its Ephrin ligands in human atherosclerosis and show a role for EPHB2 in monocyte functions independently of its EphrinB ligands. Immunohistochemical staining of human aortic sections at different stages of atherosclerosis showed that EPHB2 and its ligand EphrinB are expressed in atherosclerotic plaques and that expression proportionally increases with plaque severity. Functionally, stimulation with EPHB2 did not affect endothelial barrier function, nor did stimulation with EphrinB1 or EphrinB2 affect monocyte-endothelial interactions. In contrast, reduced expression of EPHB2 in monocytes resulted in decreased monocyte adhesion to endothelial cells and a decrease in monocyte transmigration, mediated by an altered morphology and a decreased ability to phosphorylate FAK. Our results suggest that EPHB2 expression in monocytes results in monocyte accumulation by virtue of an increase of transendothelial migration, which can subsequently contribute to atherosclerotic plaque progression.
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