fig1

Figure 1. Cellular and molecular mechanisms mediating the preventive effects of osmotin on atherosclerosis. Osmotin suppresses the proliferation of vascular ECs. It suppresses vascular inflammation, characterized as monocyte-EC adhesion, by downregulating MCP1, TNF-α, ICAM1, VCAM1, and E-selectin in ECs, and suppresses inflammatory phenotype (M1) and secretion of IL6, PTX3, and TNF-α in monocyte (Mo)-derived macrophages (Mφ). Osmotin suppresses Ox-LDL-induced foam cell formation by downregulating CD36 and ACAT1 as well as upregulating ABCA1 in Mo-derived macrophages. In VSMCs, osmotin suppresses the migration, proliferation, and production of ECM proteins, such as collagen 1, fibronectin, and matrix metalloproteinase 2. Therefore, osmotin prevents the development and instability of atheromatous plaques. EC: endothelial cells; MCP1: monocyte chemoattractant protein 1; TNF-α: tumor necrosis factor-α; ICAM1: intercellular adhesion molecule 1; VCAM1: vascular cell adhesion molecule 1; IL6: interleukin 6; PTX3: pentraxin 3; Ox-LDL: oxidized low-density lipoprotein; CD36: cluster of differentiation 36; ACAT1: acyl-coenzyme A:cholesterol acyltransferase 1; ABCA1: ATP-binding cassette transporter A1; VSMCs: vascular smooth muscle cells; ECM: extracellular matrix