© 1997 American Heart Association, Inc.
Articles |
Vitamin E Inhibits Low-Density Lipoprotein–Induced Adhesion of Monocytes to Human Aortic Endothelial Cells In Vitro
From the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (A.M., J.B.B., M.M.), Boston, Mass, and the Department of Animal and Nutritional Sciences (T.F.), University of New Hampshire, Durham.
Correspondence to Mohsen Meydani, DVM, PhD, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St, Boston, MA 02111.
Abstract Monocyte adhesion to human aortic endothelial cells
(ECs) is one of the early events in the development of atherogenesis.
ECs were used to investigate the role of vitamin E in human monocyte
adhesion to ECs in vitro. ECs incubated with 40 to 193 mg/dL of
low-density lipoprotein cholesterol (LDL) for 22 hours exhibited
increasing dose-dependent adherence for untreated, isolated human
monocytes (P<.05). ECs exposed to the highest dose of LDL
(193 mg/dL) but pretreated with 19 µmol/L 
-tocopherol for 24
hours showed a trend to lower adherence for monocytes compared with
nontreated ECs (4.4±1.2% versus 7.6±1.9%; P=.09). This
effect of vitamin E became more significant (P<.05) when
ECs were exposed to a lower level of LDL (40 mg/dL) or were pretreated
with a higher level of -tocopherol (42 µmol/L) and then
exposed to 80 mg/dL LDL. Presupplementation of ECs with 15, 19, and
37 µmol/L -tocopherol significantly (P<.05)
reduced monocyte adhesion by 6±1%, 37±6%, and 69±17%,
respectively. Levels of soluble intercellular adhesion molecule-1
(sICAM-1), one of the adhesion molecules for monocytes, increased after
incubation of ECs with LDL 80 mg/dL (4.7±0.7 versus 6.4±1.2 ng/mL,
respectively; P<.05). Treatment of ECs with -tocopherol
(42 µmol/L) significantly reduced induction of sICAM-1 by LDL to
2.2±2.3 ng/mL. After exposure to LDL, prostaglandin I2
production by ECs was diminished, whereas presupplementation of ECs
with -tocopherol partially reversed the LDL effect. Production of
interleukin-1ß was not detectable when ECs were treated with
-tocopherol, LDL, or -tocopherol followed by LDL. Our findings
indicate that vitamin E has an inhibitory effect on LDL-induced
production of adhesion molecules and adhesion of monocytes to ECs via
its antioxidant function and/or its direct regulatory effect on sICAM-1
expression.
Key Words: vitamin E • monocytes • lipoprotein • ICAM-1 • prostaglandin I2 • interleukin-1
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