Premium
Endothelial ephrin‐B2 is essential for arterial dilation
Author(s) -
Wang Rong
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.952.15
Subject(s) - nitric oxide , vasodilation , endocrinology , medicine , biology , chemistry
The Efnb2 gene encodes the cell surface protein ephrin‐B2, which is expressed in the arteries but not veins. While ephrin‐B2 plays essential roles in vascular development, its function in adult vasculature remains unknown. We have generated mice lacking Efnb2 specifically in endothelial cells ( Efnb2ΔEC ), using Tetracycline‐regulated Cre excision. About 60% of the mutants survived into adulthood and exhibited no obvious abnormalities. However, immediately following femoral artery occlusion, the Efnb2ΔEC mice exhibited lower residual foot blood flow. Foot gangrene seldom seen in controls developed in all mutants starting one day after occlusion. No obvious vascular structural abnormalities were detected to explain the blood flow defect. Acute arterial dilation induced by increased blood flow, however, in both cremaster arterioles and common carotid arteries, was impaired in Efnb2ΔEC mice. Acetylcholine‐induced arterial dilation was also reduced in Efnb2ΔEC cremasters examined. Decreased eNOS protein level and Nitric Oxide (NO) production were evident in Efnb2 −/− arterial endothelial cells. S‐Nitrosoglutathione NO, a more stable NO derivative, partially rescued gangrene progression in Efnb2ΔEC mice. Our data suggest that ephrin‐B2 plays an essential function in arterial dilation, through an NO‐mediated mechanism, and thus ephrin‐B2 is a novel molecular regulator for arterial specific dilation, crucial to vascular physiology.