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Vol. 302, Issue 2, 601-605, August 2002
Departments of Internal Medicine and Physiology and Biophysics,
University of Arkansas for Medical Sciences and Central Arkansas
Veterans Health Care System, Little Rock, Arkansas (D.L., H.C.,
J.L.M.); Department of Cardiology, University of Rome "Tor
Vergata," Rome, Italy (F.R.); Department of Forensic Medicine,
University of Uppsala, Uppsala, Sweden (To.S.); and Department of
Bioscience, National Cardiovascular Center Research Institute, Osaka
University, Osaka, Japan (Ta.S.)
LOX-1, a receptor for oxidized low-density lipoprotein (ox-LDL), plays
a critical role in endothelial dysfunction and atherosclerosis. LOX-1
activation also plays an important role in monocyte adhesion to
endothelial cells. A number of studies show that
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors
(statins) reduce total LDL cholesterol and exert a cardioprotective
effect. We examined the modulation of LOX-1 expression and its function
by two different statins, simvastatin and atorvastatin, in human
coronary artery endothelial cells (HCAECs). We observed that ox-LDL (40 µg/ml) treatment up-regulated the expression of E- and P-selectins,
VCAM-1 and ICAM-1 in HCAECs. Ox-LDL mediated these effects via LOX-1,
since antisense to LOX-1 mRNA decreased LOX-1 expression and subsequent
adhesion molecule expression. Pretreatment of HCAECs with simvastatin
or atorvastatin (1 and 10 µM) reduced ox-LDL-induced expression of
LOX-1 as well as adhesion molecules (all P < 0.05). A high concentration of statins (10 µM) was more potent than
the low concentration (1 µM) (P < 0.05). Both
statins reduced ox-LDL-mediated activation of the redox-sensitive
nuclear factor-
B (NF-B) but not AP-1. These observations indicate
that LOX-1 activation plays an important role in ox-LDL-induced
expression of adhesion molecules. Inhibition of expression of LOX-1 and
adhesion molecules and activation of NF-B may be another mechanism
of beneficial effects of statins in vascular diseases.
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