© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Albumin selectively inhibits TNF
-induced expression of vascular cell adhesion molecule-1 in human aortic endothelial cells
Linus Pauling Institute, Oregon State University, 571 Weniger Hall, Corvallis, OR 97331, USA
* Corresponding author. Tel.: +1-541-737-5078; fax: +1-541-737-5077 balz.frei{at}orst.edu
Objective: Leukocyte adhesion to, and transmigration across, the vascular endothelium are critical initiating steps in inflammation and atherosclerosis. We hypothesized that albumin, the major plasma protein, acts as an anti-inflammatory agent towards endothelial cells. Methods and Results: To test the hypothesis, we studied the effects of bovine serum albumin (BSA) on TNF
-induced expression of adhesion molecules in cultured human aortic endothelial cells (HAEC). We found that incubation of HAEC for 16 h with BSA (0.5–5%, w/v) dose-dependently inhibited TNF-induced mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1), but not intercellular adhesion molecule-1 nor E-selectin. Yeast recombinant human serum albumin exerted similar inhibitory effects on VCAM-1 expression, whereas 
-globulin was ineffective. BSA also significantly inhibited TNF-induced adhesion of monocytic THP-1 cells to HAEC in a dose-dependent manner. Furthermore, BSA strongly inhibited activation and nuclear translocation of the transcription factor, nuclear factor-
B (NF-B). For example, the physiologically relevant concentration of 5% BSA inhibited NF-B activation by 90±7%, VCAM-1 mRNA and protein expression by 81±4 and 80±13%, respectively, and THP-1 adhesion by 73±9% (n = 3). The inhibitory effect of BSA on TNF-induced VCAM-1 expression was not attenuated by inhibition of intracellular GSH synthesis. Conclusions: Our data show that physiological concentrations of albumin selectively inhibit TNF-induced upregulation of VCAM-1 expression and monocyte adhesion, most likely by inhibiting NF-B activation in a GSH-independent manner.
KEYWORDS Atherosclerosis; Cytokines; Endothelial receptors; Gene expression; Signal transduction
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