Backgrounds: Plasma level of resistin, a novel adipocyte derived cytokine, has been shown to be correlated with markers of inflammation and coronary atherosclerosis in humans. The expression of adhesion molecules on endothelial cells and subsequent adhesion of monocytes are known to be key early events in the development of atherosclerosis. Therefore, we evaluated the effect of human recombinant resistin on the expression of ICAM-1 on endothelial cells (ECs), and monocyte adhesion to ECs. We also studied putative signaling pathways, by which resistin exerts these effects. Methods and Results: Treatment of cultured human umbilical vein endothelial cells (HUVECs) with human recombinant resistin led to a significant increase in ICAM-1 expression and JNK phosphorylation, which has been shown to be one of the most important signal pathways in obesity related pathologic processes. In addition, THP-1 cell, a human monocyte cell line, adhesion to HUVECs was significantly increased in HUVECs treated with resistin compared with cells treated with control buffer (700짹56% increase in resistin 50ng/mL compared with control; P<0.01). The increased THP-1 cell adhesion to HUVECs was inhibited by ICAM-1 blocking antibodies (53짹8% decrease in ICAM-1 blocking antibodies with resistin 50ng/mL compared with resistin 50ng/mL only; P<0.01). Furthermore, treatment of HUVECs with SP600125, a JNK inhibitor, significantly inhibited both ICAM-1 expression and THP-1 cell adhesion to HUVECs (40짹20% decrease of THP-1 cell adhesion to HUVECs in SP600125 with resistin 50ng/mL compared with resistin 50ng/mL only; P<0.05), suggesting that ICAM-1 expression and cell adhesion of HUVECs to monocytes after resistin treatment, are under the regulation of JNK signal pathway. Conclusions: Resistin increases ICAM-1 expression in ECs and monocyte adhesion to ECs, through JNK activation. These results of our study suggest that resistin may play a key role in the development of atherosclerosis by promoting monocytes adhesion to ECs.