Kuhel David G, Zhu Binghua, Witte David P, Hui David Y
Center of Lipid and Arteriosclerosis Studies, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0529, USA.
Arterioscler Thromb Vasc Biol. 2002 Jun 1;22(6):955-60. doi: 10.1161/01.atv.0000017994.77066.75.
Five inbred strains of mice differing in susceptibility to diet-induced atherosclerosis were compared for neointimal hyperplasia after endothelial denudation with an epoxy resin-modified catheter probe. Results showed that all animals responded similarly to the arterial injury, with increased medial area and thickness after 14 days. In contrast, a significant strain-specific difference in neointimal formation after injury was observed. The atherosclerosis-susceptible C57L/J mice were also susceptible to injury-induced neointimal hyperplasia, and the C3H mice were resistant to both forms of vascular diseases. The 129/Sv mice, which displayed an intermediate level of diet-induced atherosclerosis, also displayed an intermediate level of injury-induced neointimal hyperplasia. Interestingly, the atherosclerosis-susceptible C57BL/6 mice were resistant to neointimal hyperplasia after endothelial denudation, whereas the atherosclerosis-resistant FVB/N mice were susceptible, displaying massive neointimal hyperplasia after arterial injury. All (C57L/JxC57BL/6)F1 hybrid mice were resistant to injury-induced neointimal hyperplasia. Moreover, N2 mice generated from backcrossing the F1 hybrid mice to the susceptible C57L/J mice displayed a range of arterial response to injury, spanning the most severe to the most resistant phenotype. These results indicate that injury-induced neointimal hyperplasia and diet-induced atherosclerosis are controlled by distinct sets of genes; the former appeared to be determined by recessive genes at > or =2 loci.
使用环氧树脂修饰的导管探头对内皮剥脱术后新生内膜增生情况进行比较，观察了对饮食诱导的动脉粥样硬化易感性不同的五种近交系小鼠。结果显示，所有动物对动脉损伤的反应相似，14天后中膜面积和厚度增加。相反，损伤后新生内膜形成存在显著的品系特异性差异。易患动脉粥样硬化的C57L/J小鼠也易发生损伤诱导的新生内膜增生，而C3H小鼠对两种形式的血管疾病均有抗性。表现出中等程度饮食诱导动脉粥样硬化的129/Sv小鼠，也表现出中等程度的损伤诱导新生内膜增生。有趣的是，易患动脉粥样硬化的C57BL/6小鼠在内皮剥脱后对新生内膜增生有抗性，而抗动脉粥样硬化的FVB/N小鼠则易感，在动脉损伤后表现出大量新生内膜增生。所有（C57L/JxC57BL/6）F1杂种小鼠对损伤诱导的新生内膜增生均有抗性。此外，将F1杂种小鼠与易感的C57L/J小鼠回交产生的N2小鼠对损伤表现出一系列动脉反应，涵盖从最严重到最抗性的表型。这些结果表明，损伤诱导的新生内膜增生和饮食诱导的动脉粥样硬化由不同的基因组控制；前者似乎由≥2个位点的隐性基因决定。
