Myoung-Sool Do, et al. Table 2. Up- or Down-Regulated Genes of Day 20/TNF-α-treated SGBS Cells Regulation Gene name Description UP DOWN RGS2 TNFSF13B CH25H Eotaxin-1 MCP-1 VCAM1 IL1F5 ADAMTS1 FN1 MMP15 PTGES Regulator of g-protein signaling 2 Tumor necrosis factor (ligand) superfamily, member 13b Cholesterol 25-hydroxylase A potent eosinophil chemoattractant Monocyte chemoattractant protein-1 Vascular cell adhesion molecule 1 isoform a precursor Interleukin 1 family, member 5 A disintegrin and metallo-protease with thrombospondin motifs-1 preproprotein Fibronectin 1 isoform 1 preproprotein Matrix metalloproteinase 15 preproprotein Prostaglandin E synthase in the array with other RNA. It is known that cross-hybridization can give a false high signal for some highly homologous gene sequences. MCP-1 is a member of the chemokine family. In vitro studies suggest that MCP-1 may contribute to the development of insulin resistance and in- duce adipocyte dedifferentiation.9 In other studies, MCP-1 mRNA expression has increased in obese mice, leading to elevated levels of plasma MCP-1 protein. The higher levels of MCP-1 protein in plasma were found to increase the CD11b-positive monocyte/macrophage population among pe- ripheral blood cells, suggesting a role for elevated MCP-1 in the vascular inflammatory process during atherosclerosis.10 Eotaxin-1 is a potent eosinophil chemoattractant that is abundant in atheromatous plaques.11 The major receptor for eotaxin-1 is CCR3, which is found on leukocytes and on some non-leukocytic cells. The expression of eotaxin-1 in human adipocytes has not yet been reported. Inflammatory cytokines induce endothe- lial VCAM1 expression, a response known to be augmented by either TRL or saturated FA.12 Con- sistent with these reports, it is demonstrated that VLDL and palmitic FA (16:0) both significantly increased VCAM1 mRNA in EC in the presence of TNF-α. Atherosclerosis involves pathological processes that include athermanous plaque formation, foam Yonsei Med J Vol. 47, No. 5, 2006 cell differentiation, inflammatory reactions, and cell proliferation. Endothelial cell activation by various inflammatory stimuli, including TNF-α, increases the adherence of monocytes, a crucial step in the development of vascular diseases. The expression of endothelial adhesion molecules, in- cluding vascular cell adhesion molecule-1, endo- thelial-leukocyte adhesion molecule-1, and intra- cellular adhesion molecule-1, plays a pivotal role in monocyte adhesion to the arterial endothe- lium.13 The expression of MCP-1, eotaxin-1, and VCAM1 in TNF-α-treated SGBS cells demon- strates that adipocytes secrete the molecules involved in atherosclerosis upon proinflammatory cytokine treatment, implying that the proinflam- matory cytokine production of overweight sub- jects might be involved in the development of atherosclerosis. Among these down-regulated genes in this study, ADAMTS1 and MMP15 are metallopro- teinases that degrade extracellular matrix macro- molecules and play important roles in tissue remodeling under many physiological and pathological conditions.14 Fibronectin (FN) is a major component of the extracellular matrix, where it is assembled from insoluble polymers and present in the blood as a soluble dimer.15 It has been reported that ADAMTS1 has ag- grecanase activity and that its activity is enhanced