Vitamin E Inhibits Low-Density Lipoprotein–Induced Adhesion of Monocytes to Human Aortic Endothelial Cells In Vitro

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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 α-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 α-tocopherol (42 μmol/L) and then exposed to 80 mg/dL LDL. Presupplementation of ECs with 15, 19, and 37 μmol/L α-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 α-tocopherol (42 μmol/L) significantly reduced induction of sICAM-1 by LDL to 2.2±2.3 ng/mL. After exposure to LDL, prostaglandin I2production by ECs was diminished, whereas presupplementation of ECs with α-tocopherol partially reversed the LDL effect. Production of interleukin-1β was not detectable when ECs were treated with α-tocopherol, LDL, or α-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.

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