© 1997 American Heart Association, Inc.
Articles |
Angiotensin II–Induced Leukocyte Adhesion on Human Coronary Endothelial Cells Is Mediated by E-Selectin
From the Departments of Internal Medicine/Cardiology and Angiology (M.G., W.A.-S., V.R.-Z., P.B., K.G., E.F.), Virchow Klinikum, Humboldt University and German Heart Institute, Berlin, the Department of Cardiovascular Surgery (M.L.), German Heart Institute, Berlin, and the Institute of Physiology (A.Z., P.G.), Free University Berlin (Germany).
Correspondence to Michael Gräfe, MD, Department of Internal Medicine/Cardiology, German Heart Institute, Augustenburger Platz 1, D-13353 Berlin, Germany.
Abstract Clinical data suggest a link between the activation
of the renin-angiotensin system and
cardiovascular ischemic events. Leukocyte
accumulation in the vessel wall is a hallmark of early
atherosclerosis and plaque progression. E-Selectin,
vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion
molecule-1 (ICAM-1) are adhesion molecules participating in mediating
interactions between leukocytes and endothelial cells
and have been found to be expressed in atherosclerotic plaques. We
investigated whether angiotensin II, the effector of the
renin-angiotensin system, influences the
endothelial expression of E-selectin, VCAM-1, and
ICAM-1. In coronary endothelial cells derived
from explanted human hearts, angiotensin II
(10-11 to 10-5 mol/L)
induced a concentration-dependent increase in E-selectin expression.
The effect was measured by cell ELISA and duplex reverse-transcription
polymerase chain reaction (RT-PCR) and reached its maximum at
10-7 mol/L. Angiotensin II induced
only a small increase in E-selectin expression in cardiac microvascular
endothelial cells. VCAM-1 and ICAM-1 were not affected
by angiotensin II stimulation. In addition, the effect of
angiotensin II–induced E-selectin expression on leukocyte
adhesion was quantified under flow conditions. Angiotensin
II (10-7 mol/L) increased leukocyte adhesion
significantly to 67% of the maximal effect by tumor necrosis
factor-
at a wall shear stress of 2 dyne/cm2. This
adhesion was found to be E-selectin dependent, as demonstrated by
blocking antibodies. The AT1-receptor
antagonist DUP 753 significantly reduced
E-selectin–dependent adhesion, whereas the AT2-receptor
antagonist PD 123177 had no inhibitory effect.
In addition, only AT1-receptor, but not
AT2-receptor, mRNA could be detected by RT-PCR in
coronary endothelial cells. Therefore, it is
suggested that AT1 receptors mediate the effects of
angiotensin II on E-selectin expression and leukocyte
adhesion on coronary endothelial cells.
Key Words: endothelial cell • angiotensin II • E-selectin
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