Circulation Research. 2001;89:477-479
Published online before print August 30, 2001, doi: 10.1161/hh1801.097034
Published online before print August 30, 2001, doi: 10.1161/hh1801.097034
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© 2001 American Heart Association, Inc.
Reports |
Angiopoietin-1 Reduces VEGF-Stimulated Leukocyte Adhesion to Endothelial Cells by Reducing ICAM-1, VCAM-1, and E-Selectin Expression
From the National Creative Research Initiatives Center for Endothelial Cells (I.K., S.O.M., G.Y.K.) and Departments of Internal Medicine (S.K.P.) and Pharmacology (S.W.C.), Chonbuk National University School of Medicine, Chonju, Republic of Korea.
Correspondence to Gou Young Koh, MD, PhD, National Creative Research >Initiatives Center for Endothelial Cells, Department of Life Science, Pohang University of Science and Technology, San 31, Hyoja-Dong, Pohang, 790-784, Republic of Korea. E-mail gykoh{at}postech.ac.kr
Abstract
Vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang1) are potent vasculogenic and angiogenic factors that hold promise as a means to produce therapeutic vascularization and angiogenesis. However, VEGF also acts as a proinflammatory cytokine by inducing adhesion molecules that bind leukocytes to endothelial cells, an initial and essential step toward inflammation. In the present study, we used human umbilical vascular endothelial cells (HUVECs) to examine the effect of Ang1 on VEGF-induced expression of three adhesion molecules: intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Interestingly, Ang1 suppressed VEGF-induced expression of these adhesion molecules. Furthermore, Ang1 reduced VEGF-induced leukocyte adhesion to HUVECs. These results demonstrate that Ang1 counteracts VEGF-induced inflammation by reducing VEGF-induced endothelial adhesiveness.
Key Words: vascular endothelial growth factor • angiopoietin • adhesion • inflammation
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