To this end, in this study, we aimed to investigate the effects of various concentrations of estradiol, either alone or after mimicking a low-grade inflammation state that occurs post-menopause in established atherosclerosis, on the expression of molecules involved in atherosclerosis plaque vulnerability (MCP-1, PDGF-β, ADAMTS-4, MMP-2, MMP-9, TIMP-1, TIMP-2, and OPG/RANK/RANKL expression) and MMP activity, using human aortic endothelial cells (HAECs), which offer the best in vitro model system for studying CVD. This evidence concerns the gene CCL2 and atherosclerosis.