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Abstract 469: Air Pollution Promotes CD36-Dependent Accumulation of Oxidized Lipids


 BACKGROUND:
 The adverse effect of air pollution on cardiovascular disease such as atherosclerosis has long been proposed. We previously reported that exposure to fine particular matter <2.5 microns (PM2.5) increased oxidized lipids in the lung and atherosclerotic plaque burden in the aorta. However, it is currently unclear how signals emanating from the lung contribute to systemic and vascular effects given the fact that the vast majority of PM2.5 particles do not cross the lung barrier.
 
 
 Methods and Results:
 Using an in vivo whole body exposure system, ApoE-/- mice were exposed to filter air (FA) or concentrated PM2.5 for 6 months. Exposure to PM2.5 increased expression of CD36, a scavenger receptor responsible for oxidized lipid uptake, on macrophages. In addition, CD36-dependent phagocytosis was also enhanced in macrophages isolated from ApoE-/- mice exposed to PM2.5. There were increased CD36-expressing macrophages in the plaque of PM2.5-exposed ApoE-/- mice. In line with that, inhalation of PM2.5 increased 7-ketocholesterol, the dominant form of oxidized lipids, in thoracic aorta of ApoE-/- mice. Exposure to PM2.5 promoted the formation of foam cell as demonstrated by increased lipid droplets formation inside macrophages after incubation with oxLDL, while knockdown of CD36 by siRNA could at least partially block this effect. Consistently, macrophages isolated from CD36-/- mice were less sensitive to oxLDL-induced form cell formation, compared to wild-type macrophages.
 
 
 CONCLUSIONS:
 Air pollution accelerates atherosclerosis through promoting CD36-dependent accumulation of oxidized lipids. Our data suggest a role for CD36 in lipid dysregulation and foam cell formation in atherosclerosis.
