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We previously reported that the apolipoprotein (apo) B48-carrying lipoproteins obtained from apoE knockout ( apoE    − / −  ) mice, so called E − /B48 lipoproteins, transformed mouse macrophages into foam cells and enhanced the phosphorylation of eukaryotic translation initiation factor 2  α   (eIF-2  α  ). Furthermore, the eIF-2  α   phosphorylation inhibitor, 2-aminopurine (2-AP), attenuated E − /B48 lipoprotein-induced foam cell formation. The present report studied the effect of 2-AP on atherosclerosis in  apoE    − / −   mice. Our results showed that the level of food intake, bodyweight, plasma cholesterol, and triglycerides was comparable in  apoE    − / −   mice treated with or without 2-AP. However, the mean size of atherosclerotic lesions in the aorta sinus as well as the surface area of the entire aorta of 2-AP-treated  apoE    − / −   mice were reduced by about 55% and 39%, respectively, compared to samples from untreated control  apoE    − / −   mice. In addition, the 2-AP-treated  apoE    − / −   mice showed a significant decrease in glucose-regulated protein 78 (GRP78) and phosphorylated eIF-2  α   in their aortic samples as compared to levels in untreated control  apoE    − / −   mice. These observations suggest that endoplasmic reticulum stress is a causal mechanism for the development of atherosclerosis in  apoE    − / −   mice and that therapeutic strategies can be developed for using eIF-2  α   phosphorylation inhibitors, such as 2-AP, to prevent or treat atherosclerosis.

Inhibition of Endoplasmic Reticulum Stress and Atherosclerosis by 2-Aminopurine in Apolipoprotein E-Deficient Mice