**3. Actions of lipoprotein-associated phospholipase A2**

We can think about Lp-PLA2 as a friend and foe at the same time. On the one hand, it functions as PAF-AH, which hydrolyzes inflammatory mediator PAF, inhibits foam cell formation, enhances cholesterol efflux in macrophages, and exerts its atheroprotective role [16].

On the other hand, Lp-PLA2 has a proatherogenic role. Lp-PLA2 relates to a number of different proatherogenic biological processes. Lp-PLA2 hydrolyzes oxidized phospholipids on modified LDL particles within the arterial intima, and thus contributes to the initiation and progression of atheroma. Lp-PLA2 is produced by macrophages and foam cells within atherosclerotic plaque. Its expression is mainly confined to plaque areas with massive lipid accumulation and leukocyte infiltration, cellular necrosis, and calcification, suggesting that Lp-PLA2 is a marker for rupture-prone plaque [16]. The amount of Lp-PLA2 and its by-product, lysophosphatidyl‐ choline in the coronary circulation is proportional to the extent of the atheroma and indirectly affects local endothelial function [17]. Proatherogenic activities of lysophosphatidylcholine are: expression of adhesion molecules; upregulation of cytokines and CD40 ligand by T-cells, cytotoxic at concentrations higher than 30–50 µM; stimulation of macrophage proliferation; release of arachidonic acid from endothelial cells; induction of MCP-1 and genes for growth factors; release of myeloperoxidase; migration of vascular smooth muscle cells; chemoattrac‐ tant for monocytes, macrophages, and T-cells; induction of apoptosis in smooth muscle cells and macrophages; involvement in the antigenicity of oxidized LDL; inhibition of endotheliumderived nitric oxide [18-20]. Furthermore, oxFFAs promote atherosclerosis by direct and indirect increasing of oxidative stress and the presence of oxidized LDL and other lipoproteins in the plasma and arterial walls, thereby initiating fatty streak formation [21].
