Abstract 8907: Fatty-Acid-Binding Protein 3 as a Novel Inducer of Adhesion Molecules in Atherosclerosis

Abstract

Introduction: Cardiovascular disease is accompanied by a considerable degree of morbidity and mortality, and the pathogenesis is complex. The fatty-acid-binding protein 3 (FABP-3) is a cytoplasmic protein and can be released from injured myocardium. We had demonstrated that FABP-3 was an independent predictor for cardiovascular outcomes in the patients with stable coronary artery disease (CAD). However, the mechanisms of FABP-3 in atherosclerosis were still unknown. Here we supposed that FABP-3 could lead to atherogenesis via activating the adhesion molecules. Methods and Results: Human coronary endothelial cells (HCAECs) and mononuclear cells (MNCs) cultured from CAD patients and healthy subjects were used for the in vitro study. The ox-LDL and TNF-α were used as stimulators in the in vitro experiments. The expressions of adhesion molecule were evaluated by Western blot analysis. MNCs from CAD patients had higher expressions of FABP-3 than those from healthy subjects. In addition, FABP-3 could be further up-regulated by ox-LDL and TNF-α stimulations in both MNCs from CAD patients and healthy subjects. Exogenous of FABP-3 could directly induce the adhesion molecules including integrin β2, integrin α4, and P-selectin glycoprotein ligand 1 expressions in MNCs from CAD patients and healthy subjects. Nevertheless, direct treatments of FABP-3 did not upregulate the adhesion molecules in HCAECs. Also, the adhesiveness of FABP-3-induced adhesiveness of HCAECs to THP-1 monocytic cells was not enhanced. Conclusions: According to the above results, we suggested that FABP-3 could directly lead to the atherogenesis via the MNC activation instead of endothelial cell activation. The findings of the serial studies may not only elucidate the prognostic role of plasma FABP-3 levels in patients with CAD but define the role of FABP-3 on the pathogenesis of atherosclerosis especially its influence in MNCs. The study might clarify the clinical impact of FABP-3 and as a potential novel therapeutic target for atherosclerosis.