Guy Ella, Kuchibhotla Sai, Silverstein Roy, Febbraio Maria
Department of Medicine, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, United States.
Atherosclerosis. 2007 May;192(1):123-30. doi: 10.1016/j.atherosclerosis.2006.07.015. Epub 2006 Aug 17.
We previously determined that absence of CD36 inhibited atherosclerosis lesion development in 12-week Western diet fed apoE degrees 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 degrees and CD36 degrees /apoE degrees 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 degrees /apoE degrees mice. Most impressive was the difference in gross appearance of the aortas at 35 weeks: apoE degrees aortas were sclerotic and nearly occluded by lesion, whereas aortas from CD36 degrees /apoE degrees 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 degrees model.
我们先前确定，在喂食西方饮食12周的载脂蛋白E缺陷型小鼠中，CD36缺失可抑制动脉粥样硬化病变发展，这主要归因于巨噬细胞CD36的缺失。在疾病后期，由于病变发展的渐进性和其他因素的参与，这种效应可能会消失。然而，病变发展仍以巨噬细胞募集和泡沫细胞形成为特征，因此，由于CD36缺失导致的脂质积累延迟也可能会继续延缓病变发展。本研究的目的是确定CD36缺失是否继续抑制病变形成。背景匹配的载脂蛋白E缺陷型和CD36缺陷型/载脂蛋白E缺陷型小鼠喂食西方饮食长达35周。在20周和35周时，CD36缺陷型/载脂蛋白E缺陷型小鼠的病变面积分别减少了25%和35%。最令人印象深刻的是35周时主动脉外观的差异：载脂蛋白E缺陷型主动脉硬化，几乎被病变阻塞，而CD36缺陷型/载脂蛋白E缺陷型小鼠的主动脉病变较小，更呈点状。我们得出结论，即使在载脂蛋白E缺陷型模型的疾病后期，CD36缺失仍能继续减轻病变负担。
