Continued inhibition of atherosclerotic lesion development in long term Western diet fed CD36°/apoE° mice


      We previously determined that absence of CD36 inhibited atherosclerosis lesion development in 12-week Western diet fed apoE° mice, and this was due largely to absence of macrophage CD36. It is possible that at later stages of disease this effect would be lost due to the progressive nature of lesion development and involvement of other factors. However, lesion development continues to be characterized by recruitment of macrophages and foam cell formation, thus it is also possible that delay in lipid accumulation as a result of absence of CD36 would continue to retard lesion development. The objective of this study was to determine if absence of CD36 continued to inhibit lesion formation. Background matched apoE° and CD36°/apoE° mice were fed a Western diet for up to 35 weeks. At 20 and 35 weeks, lesion area was 25 and 35% less, respectively, in CD36°/apoE° mice. Most impressive was the difference in gross appearance of the aortas at 35 weeks: apoE° aortas were sclerotic and nearly occluded by lesion, whereas aortas from CD36°/apoE° mice had smaller lesions that were more punctate. We conclude that absence of CD36 continues to reduce lesion burden even at late stages of disease in the apoE° model.


      apoE° (apolipoprotein E knock out), CD36° (CD36 knock out), HDL (high density lipoprotein), HIV (human immunodeficiency virus), IACUC (institutional animal care and use committee), LDL (low density lipoprotein), LOX-1 (lectin-like low density lipoprotein receptor), MPO (myeloperoxidase), NEFA (non-esterified fatty acids), PBS (phosphate buffered saline), PCR (polymerase chain reaction), PPAR (peroxisome proliferator activated receptor), SRA-I/II (scavenger receptor A I/II)


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