|Goodwin, Van -|
|Burris, Ramona -|
|Nagarajan, Shanmugam -|
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: February 11, 2009
Publication Date: April 1, 2009
Repository URL: http://www.fasebj.org.libproxy.uams.edu/content/vol23/1_MeetingAbstracts/aindex.shtml#A
Citation: Goodwin, V.B., Burris, R.L., Nagarajan, S. 2009. Soy diet inhibits expression of inflammation-induced vascular cell adhesion molecules in endothelial cells [abstract]. FASEB J. 23(1_MeetingAbstracts):924.5. Interpretive Summary: Heart attack is caused by reduced blood flow to the heart. This is due to the thickening of blood vessels, also known as atherosclerosis. Asian populations consume diets high in soy. Studies have suggested that the decreased rate of heart disease in Asians may be due to their dietary consumption of soy. We are interested in determining if soy can reduce the incidence of heart disease. In this study we examined the effect of soy diet on cell types lining the blood vessels, also known as endothelial cells. Our study showed that mice fed soy diet have reduced expression of cell adhesion molecules in the aorta than. This study also demonstrated that soy phytochemicals contribute to the protective effects of soy diet. In our future studies we will determine any additional mechanisms contributing to the protective effect of soy.
Technical Abstract: Recently we reported that dietary soy attenuated atherogenesis in apolipoprotein E knockout (apoE-/-) mice. However, the molecular mechanisms contributing to the atheroprotective effect of soy-based diets is not clear. Since interactions between endothelial cells and monocytes play a pivotal role in the initiation of atherosclerosis, we hypothesize that components in soy diet prevent monocyte adhesion to endothelial cells by inhibiting vascular cell adhesion molecule expression on endothelial cells. Genistein, a major soy isoflavone, inhibited expression of TNF-alpha-induced vascular adhesion molecules CD62E (E-selectin) and CD106 (VCAM-1) in HUVEC cells in a concentration-dependent (1-100 µM) manner, with no effect on CD54 (ICAM-1) expression. Interestingly, equol, a metabolite of the soy isoflavone daidzein produced by gut microflora, also showed significant inhibition of inducible CD62E and CD106 expression. The effect of soy feeding on expression of CD106 was further addressed in apoE-/- mice. Quantitative RT-PCR analyses of proximal aorta showed reduced expression of CD106 in soy-fed compared to casein-fed mice. These findings suggest that the atheroprotective effect of soy diet is mediated, in part, by inhibition of vascular cell adhesion molecule expression that could lead to reduced monocyte adhesion and migration, an early event in atherogenesis.