Abstract
To clarify the physiological role of CD36, we analyzed the gene abnormalities of CD36 deficient subjects and the role of CD36 as an oxidized LDL receptor by using monocyte-derived macrophages from normal and two CD36-deficient subjects. We further analyzed the expression of CD36 in human atherosclerotic tissues and the regulation of CD36 by oxLDL in vitro. Scatchard analysis of 125I-OxLDL binding showed a linear plot and the maximum binding was lower by approximately 40% in the macrophages from subj ects with CD36 deficiency than those from normal controls. Competition studies showed that the uptake of 125I-OxLDL was suppressed by OKM5, an antibody against CD36, by 53% in normal control macrophages, but not in the CD36-deficient macrophages. After incubation with OxLDL for 24h, cholesteryl ester mass accumlation was reduced in the macrophages from CD36-deficient subjects than those from normal controls. These results suggest that CD36 is one of the physiological receptors for OxLDL. In immunochemical analysis of human aortic tissues, the expression of CD36 is very low in normal aorta, while the expression of CD36 in atheromatous plaque, CD36 is highly expressed in macrophages. In vitro assay, CD36 is upregulated by the addition of oxidized LDL in medium after 24 hours incubation. From these observations, CD36 is suggested that it plays an important role on foam cell formation of macrophages in atherosclerosis.
