(Circulation. 2000;101:235.)
© 2000 American Heart Association, Inc.
Brief Rapid Communications |
Modulation of Vascular Inflammation In Vitro and In Vivo by Peroxisome Proliferator–Activated Receptor-
Activators
From the Department of Internal Medicine (V.P., H.D.W., J.T.W., E.T.H.Y.) and Institute of Molecular Medicine for the Prevention of Human Diseases (E.T.H.Y.), University of Texas Health Science Center, and Texas Heart Institute (V.P., J.T.W., E.T.H.Y.), St Luke’s Episcopal Hospital, Houston.
Correspondence to Edward T.H. Yeh, MD, Department of Internal Medicine, 6431 Fannin, Suite 4200, UT-Houston HSC, Houston, TX 77030.
Background—Peroxisome
proliferator–activated receptor-
(PPAR) is expressed in
atherosclerotic plaques and in endothelial cells. The
possible effects of PPAR activators on
endothelial activation and inflammatory response within
the plaque are currently unknown.
Methods and Results—We tested the hypothesis that PPAR
activators inhibit vascular cell adhesion molecule (VCAM-1)
and intercellular adhesion molecule (ICAM-1) expression in cultured
endothelial cells (evaluated by flow cytometry) and
homing of monocyte/macrophages to atherosclerotic plaques in
vivo. In endothelial cells, the PPAR agonists
troglitazone at 100 µmol/L and
15-deoxy-
12,14-prostaglandin
J2 (15d-PGJ2) at 20 µmol/L markedly attenuated the
tumor necrosis factor–induced expression of VCAM-1 and ICAM-1. A
significant inhibition of VCAM-1 expression was also evident at 5 and
10 µmol/L 15d-PGJ2 and 20 µmol/L troglitazone. Expression
of E-selectin and PECAM-1 was not altered. To confirm the biological
relevance of these results, we assessed the effects of troglitazone on
monocyte/macrophage homing to atherosclerotic plaques in
apoE-deficient mice. A 7-day treatment with troglitazone (400 mg/kg)
significantly reduced monocyte/macrophage homing to
atherosclerotic plaques (236±77 versus 177±43 macrophages,
P=0.03); an even more striking inhibition was found at
3200 mg/kg troglitazone (344±76 versus 172±83 macrophages,
P=0.005).
Conclusions—PPAR activators inhibit expression of
VCAM-1 and ICAM-1 in activated endothelial
cells and significantly reduce monocyte/macrophage homing to
atherosclerotic plaques. These findings suggest that PPAR
activators, currently used in treatment of type II
diabetes, may have beneficial effects in modulating inflammatory
response in atherosclerosis.
Key Words: cell adhesion molecules • receptors • atherosclerosis
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