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Reduced adult endothelial cell EphB4 function promotes venous remodeling
Caroline C Jadlowiec1, Amanda Feigel, Chenzi Yang
1The Interdepartmental Program in Vascular Biology and Therapeutics and the Department of Surgery, Yale University School of Medicine, New Haven, CT 06520, USA.
American Journal of Physiology. Cell Physiology
|December 28, 2012
Summary
Reduced EphB4 signaling in venous endothelial cells (EC) impairs their function, leading to increased vein wall thickening. This suggests EphB4 loss contributes to vein graft adaptation issues.
Area of Science:
- Vascular Biology
- Cell Biology
- Regenerative Medicine
Background:
- EphB4 expression is reduced during vein graft adaptation, correlating with venous wall thickening.
- EphB4 may play a role in normal adult venous endothelial cell (EC) function and vein graft adaptation.
Purpose of the Study:
- To investigate the functional significance of EphB4 in adult venous EC.
- To determine the role of EphB4 in vein graft adaptation.
Main Methods:
- Isolated EC from EphB4(+/+) and EphB4(+/-) mice for in vitro functional assays (proliferation, migration, nitric oxide synthesis, chemokine production).
- Utilized a mouse vein graft model to correlate in vitro findings with in vivo outcomes.
- Assessed smooth muscle cell (SMC) proliferation and migration using EC-conditioned medium.
Main Results:
- EphB4(+/-) EC showed reduced proliferation, migration, and nitric oxide (NO) production.
- EphB4(+/-) EC exhibited increased VEGF-A, PDGF-BB, and TGF-β1 secretion.
- Conditioned medium from EphB4(+/-) EC promoted SMC proliferation and migration.
- Vein grafts and EphB4(+/-) EC shared similarities in VEGF-A and eNOS expression.
Conclusions:
- Reduced EphB4 function in venous EC is linked to a proangiogenic and mitogenic phenotype.
- Loss of EphB4 in venous EC leads to increased SMC mitogens and reduced NO production, contributing to vein graft neointima thickening.
- EphB4 is active in adult venous EC, and its loss is implicated in vein graft adaptation processes.
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