Possible Regulation of Platelets by Native and Modified Low Density Lipoprotein-Cholesterol Particles

An excess number of low density lipoprotein-cholesterol (LDL-C) particles is an independent risk for a cardiovascular event in the future.LDL particles diffused into the developing atherosclerotic plaques bind to proteoglycans in the intima, become oxidized and phagocytosed to macrophages.This causes the generation of foam cells, which aggravate the generation of fatty streaks and induce platelet attachment. 1)It is highly probable that platelets may have contact with oxidized LDL (oxLDL).2)3) Several results describe that oxLDL can be exposed to circulating blood or can even be formed in plasma at sites of oxidative stress.Platelets express a series of receptors that specifically recognize oxLDL, such as CD36 and scavenger receptor A (SRA).oxLDL-bound CD36 and SRA induce phosphorylation of p38 MAP kinase (MAPK), which in turn triggers the production of thromboxane A2 through the activation of a cytoplasmic type of phospholipase A2. 4) Thus, the stimulation with oxLDL enables platelets to induce aggregation independently or with other stimulatory signals such as adenosine diphosphate (ADP), collagen or thrombin in a synergistic manner.Unlike oxLDL, native and non-oxLDL particles are functionally inert and little has been described regarding the activity of native LDL on any type of cells that may contribute to the development of athero-