期刊文献+

载脂蛋白E基因缺陷对小鼠主动脉壁caveolin-1表达的影响

Affection of ApoE Gene-deficiency on the Expression of Caveolin-1 in the Wall of Artery
下载PDF
导出
摘要 目的探讨高脂喂养的C57BL/6J小鼠和普饲喂养的apoE基因缺陷(apoE-/-)小鼠(品系为C57BL/6J)caveolin-1表达的差异。方法取apoE-/-小鼠作为研究对象,以普饲和高脂喂养的C57BL/6J小鼠为对照组,测定各组小鼠血脂和主动脉壁斑块的变化,Western-blotting检测caveolin-1在主动脉的表达。结果普饲喂养的apoE-/-组和高脂喂养的C57BL/6J组血脂水平较普饲喂养的C57BL/6J组明显升高;普饲喂养的apoE-/-组的主动脉形成明显的斑块,高脂喂养C57BL/6J组没有形成斑块,但血管壁平滑肌细胞出现增殖,普饲喂养的C57BL/6J组未见明显变化。Wester-blotting检测显示普饲喂养的apoE-/-小鼠和高脂喂养的C57BL/6J小鼠caveolin-1的表达与普饲喂养的C57BL/6J小鼠比较明显减弱。结论血管壁caveolin-1的表达下调可能是apoE-/-小鼠动脉粥样硬化形成的重要原因。 Objective To observe the expression of caveolin-1 in the apoE-deficient mice. Methods Male C57BL/6J mice and apoE-deficient mice were devided into apoE-deficient and control group mice,the latter were further divided into 2 subgroups common feedstuff and high-fat(n=10).The serum total cholesterol, triglyceride,high and low density cholesterol were determined.The change of aortic wall and plaque lesion were observed.Caveolin-1 was assayed by western-blotting. Results The serum levels of total cholesterol ,triglyceride,and low density cholesterol in the apoE-deficient mice and high-fat were elevated significantly compared with those in the normal mice, apoE-deficient mice developed plaque in the artery, but not high-fat mice. The expression of caveolin-1 in aortic wall in the apoE-deficient mice is decreased compared with those in the normal mice. Conclusion The decrease of expression of caveolin-1 in aortic of apoE-deficient mice is the main cause of atherositic formation.
出处 《南华大学学报(医学版)》 2005年第3期295-298,共4页 Journal of Nanhua University(Medical Edition)
基金 国家自然基金资助项目(NO30171084 39970847).
关键词 CAVEOLIN-1 动脉粥样硬化 apoE基因缺陷 caveolin-1 atherosclerosis apoE gene-deficient
  • 相关文献

参考文献10

  • 1Rothberg KG,Heuser JE,Donzell WC.et al.Caveolin,protein component of caveolae membrane coats[J].Cell,1992,68:673—682.
  • 2Maor I,Aviram M.Oxidized low density lipoprotein leads to macmphage accumulation of unesterified cholesterol as a result of lysosomal trapping of the lipoprotein hydrolyzed cholesteryl ester[J].J Lipid Res,1994,35;803-819.
  • 3Lange Y,Steck TL.The role of intracellular cholesterol transport in cholesterol homeostasis[J].Trans Cell Biol,1996,6(6):205—208.
  • 4Mahley RW.Apoliprotein E:cholesterol transport protein with expanding role in cell biology[J].Science,1998,240:622—630.
  • 5Kruth HS,Skarlatos SI,Gaynor PM.et al.Production of cholesterol-enriched nascent high density lipoproteins by human monocytederived macrophages is a mechanism that contributes to macophage cholesterol efflux[J].J Biol Chem,1994,269(39):24511—24518.
  • 6张春妮,Hakamata Hideki,Sakaguchi Hisashi,Suzuki Hirosh,Miyazaki Akira,庄一义,Horiuchi Seikoh.载脂蛋白E-基因敲除鼠VLDL和IDL在动脉硬化中的作用[J].南京大学学报(自然科学版),1999,35(2):180-185. 被引量:1
  • 7Cader AA, Steinberg FM, Mazzone T, et al.Mechanism of enhanced macrophage ApoE secretion by oxidized LDL [ J ]. J Lipid Res,1997, 38:981-991.
  • 8Plum AS, Jonathan D Smith, Tony Hayek, et al. Severe hyperc2 holesterolemia and atheroslerosis in apolipoprotein E-deficient mice created by homologous recombination in ES Cells[J]. Cell , 1992 , 71 (10) :343 - 353.
  • 9Zhang Sunny H, Reddick RL, Piedrahita JA, et al. Spon2taneous hypercholesterolemia and arterial lesions in mice lacking aopolipoprotein E[J]. Science , 1992 ,258 (10) :468 - 471.
  • 10Yutaka Nakashima, Audrew S Plump, Elaine W Raines, et al. ApoE- deficient mice develop lesions of all phases of atheroslerosis throughout the arterial tree[J]. Arteriosclerosis and Thrombosis , 1994 , 14 ( 1 ) : 133 - 140.

二级参考文献1

  • 1Zhang S H,Science,1992年,258卷,468页

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部