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首页> 外文期刊>American Journal of Pathology: Official Publication of the American Association of Pathologists >Aggressive very low-density lipoprotein (VLDL) and LDL lowering by gene transfer of the VLDL receptor combined with a low-fat diet regimen induces regression and reduces macrophage content in advanced atherosclerotic lesions in LDL receptor-deficient
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Aggressive very low-density lipoprotein (VLDL) and LDL lowering by gene transfer of the VLDL receptor combined with a low-fat diet regimen induces regression and reduces macrophage content in advanced atherosclerotic lesions in LDL receptor-deficient

机译：通过VLDL受体基因转移与低脂饮食方案相结合的攻击性极低密度脂蛋白（VLDL）和LDL降低可导致LDL受体不足的晚期动脉粥样硬化病变中的回归并降低巨噬细胞含量

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Very low-density lipoprotein (VLDL) and LDL plasma levels are associated with cardiovascular mortality. Whereas VLDL/LDL lowering causes regression of early atherosclerotic lesions, less is known about the effects of aggressive lipid lowering on regression of advanced complex lesions. We therefore investigated the effect of VLDL/LDL lowering on pre-existing lesions in LDL receptor-deficient mice. Mice fed a high-fat diet for 16 weeks developed advanced lesions with fibrous caps, necrotic cores, and cholesterol clefts in the brachiocephalic artery. After an additional 14 weeks on a low-fat diet, plasma cholesterol levels decreased from 21.0 +/- 2.6 to 8.4 +/- 0.6 mmol/L, but lesions did not regress. Levels of VLDL/LDL were further lowered by using a helper-dependent adenovirus encoding the VLDL receptor (HD-Ad-VLDLR) under control of a liver-selective promoter. Treatment with HD-Ad-VLDLR together with a low-fat diet regimen resulted in reduced lesion size (cross-sectional area decreased from 146,272 +/- 19,359 to 91,557 +/- 15,738 microm2) and an 89% reduction in the cross-sectional lesion area occupied by macrophages compared to controls. These results show that aggressive VLDL/LDL lowering achieved by hepatic overexpression of VLDLR combined with a low-fat diet regimen induces regression of advanced plaques in the brachiocephalic artery of LDL receptor-deficient mice.
机译：低密度脂蛋白（VLDL）和LDL血浆水平与心血管疾病死亡率相关。 VLDL / LDL降低导致早期动脉粥样硬化病变消退，而主动降脂对晚期复杂病变消退的影响知之甚少。因此，我们研究了VLDL / LDL降低对LDL受体缺陷型小鼠中预先存在的病变的影响。喂食高脂饮食16周的小鼠出现了进展性病变，在头颅动脉中出现了纤维帽，坏死核心和胆固醇裂痕。在低脂饮食下再维持14周后，血浆胆固醇水平从21.0 +/- 2.6降至8.4 +/- 0.6 mmol / L，但病变并未消退。通过在肝脏选择性启动子的控制下使用编码VLDL受体的辅助依赖性腺病毒（HD-Ad-VLDLR），可进一步降低VLDL / LDL的水平。 HD-Ad-VLDLR与低脂饮食方案一起治疗可减少病变大小（横截面积从146,272 +/- 19,359微米减少到91,557 +/- 15,738平方微米），并且横截面减少89％与对照相比，巨噬细胞占病变面积。这些结果表明，通过肝脏过度表达VLDLR与低脂饮食方案相结合可实现VLDL / LDL降低，从而导致LDL受体缺陷型小鼠的头颅动脉中的晚期斑块消退。

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