THE FATE OF LIPOPROTEIN CHOLESTEROL ENTERING THE ARTERIAL-WALL

Recent findings have helped to explain the fate of cholesterol enterin g the arterial wall. LDL can undergo both fusion and aggregation. Thes e changes may cause increased retention of LDL in lesion connective ti ssue matrix and LDL uptake by macrophages. In the cornea, apparent fus ion of LDL occurs in the absence of macrophages. Mast cells may be imp ortant in LDL fusion, as mast cell-derived proteases can induce fusion of LDL through proteolysis of apolipoprotein B. LDL in arterial wall atherosclerotic lesions was found to be sialic acid-poor and ceramide- enriched. These chemical changes promote LDL aggregation. Processes th at may function to remove cholesterol from the arterial wall have been reported. Macrophage-produced apolipoprotein E can mediate macrophage cholesterol efflux and macrophages can convert cholesterol to 27-oxyg enated products that macrophages excrete. Alternately, another oxygena ted sterol, 7-ketocholesterol, impairs macrophage cholesterol efflux. In addition, mast-cell derived chymase proteolyses HDL and reduces its capacity to stimulate cholesterol efflux.