Gene Chip Analysis for Artery of Rats with Atherosclerosis_West China Medical Journal

Authors：

 ZHONGWu , RONGHua , CHENMu-hu , YUPing-gui , WANGLiang ,  HEYan-zheng

Department of Emergency, Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan 646000, P. R. China;

Corresponding author：

HEYan-zheng, Email: heyanzheng@163.com

Keywords：

Gene chip; Atherosclerosis; Rats

DOI：

10.7507/1002-0179.20140264

Video：

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Abstract Full text Figures/Tables Video References Cited by

Objective To investigate the pathogenesis of atherosclerosis (AS) by detecting different expression genes between normal Wistar rats and rats with atherosclerosis through the technology of gene chip. Methods The rats were treated with standard diet with saline injection (control group) or high-cholesterol diet with vitamin D3 injection and balloon injury (model group). Total cholesterol (TC) and triglyeride (TG) in serum were detected 90 days later to ensure the success of establishment of the atherosclerosis model. Abdominal aorta was isolated and stained with HE. Total RNA was isolated from the aorta for gene chip analysis to explore the differential gene expression. Results Compared with the control group, the TC and TG level in the model group were highly advanced (P<0.05). AS model was confirmed by pathological observation. Gene chip detection showed that 511 genes were up-regulated and 1 219 ones were down-regulated which were interrelated with lipid metabolism, inflammatory reaction, oxidative stress and apoptosis as well. Conclusion The expression change with multiple gene in AS suggests that the nosogenesis of AS is adjusted and controlled complicatedly. Intensive study of some important genes will contribute to the prevention and improvement of prognosis of AS.

Citation： ZHONGWu, RONGHua, CHENMu-hu, YUPing-gui, WANGLiang, HEYan-zheng. Gene Chip Analysis for Artery of Rats with Atherosclerosis. West China Medical Journal, 2014, 29(5): 867-870. doi: 10.7507/1002-0179.20140264 Copy

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8.	Satterthwaite G, Francis SE, Suvarna K, et al. Differential gene expression in coronary arteries from patients presenting with ischemic heart disease:further evidence for the inflammatory basis of atherosclerosis[J]. Am Heart J, 2005, 150(3):488-499.
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11.	卢次勇, 凌文华, 马静, 等. 氧化型低密度脂蛋白诱导血管内皮细胞基因表达谱的改变[J]. 中国动脉硬化杂志, 2002, 10(6):483-486.
12.	顾菲菲, 高炜, 蒋捷, 等. 基因芯片在同型半胱氨酸诱导动脉粥样硬化基因表达谱变化中的应用[J]. 中国动脉硬化杂志, 2004, 12(4):433-437.
13.	Li H, Lewis A, Brodsky S, et al. Homocysteine induces 3-hydroxy-3-methylglutaryl coenzyme a reductase in vascular endothelial cells:a mechanism for development of atherosclerosis?[J]. Circulation, 2002, 105(9):1037-1043.
14.	Katsuda S, Kaji T. Atherosclerosis and extracellular matrix[J]. J Atheroscler Thromb, 2003, 10(5):267-274.
15.	Vivanco F, Martín-Ventura JL, Duran MC, et al. Quest for novel cardiovascular biomarkers by proteomic analysis[J]. J Proteome Res, 2005, 4(4):1181-1191.
16.	Bengtsson E, To F, Grubb A, et al. Absence of the protease inhibitor cystatin C in inflammatory cells results in larger plaque area in plaque regression of apoE-deficient mice[J]. Atherosclerosis, 2005, 180(1):45-53.

1. Finn AV, Nakano M, Narula J, et al. Concept of vulnerable/unstable plaque[J]. Arterioscler Thromb Vasc Biol, 2010, 30(7):1282-1292.
2. Fishbein MC. The vulnerable and unstable atherosclerotic plaque[J]. Cardiovasc Pathol, 2010, 19(1):6-11.
3. Fraser JK, Wulur I, Alfonso Z, et al. Fat tissue:an underappreciated source of stem cells for biotechnology[J]. Trends Biotechnol, 2006, 24(4):150-154.
4. 郭延松, 吴宗贵, 杨军柯, 等. 三种大鼠动脉粥样硬化模型复制方法的比较[J]. 中国动脉硬化杂志, 2003, 11(5):465-469.
5. 杨晓玲, 赵迅霞, 王菲, 等. 实验大鼠动脉粥样硬化模型的建立[J]. 宁夏医学院学报, 2007, 29(4):350-351, 450.
6. Ross R. Atherosclerosis is an inflammatory disease[J]. Am Heart J, 1999, 138(5 Suppl):S419-S420.
7. Zhao B, Stavchansky SA, Bowden RA, et al. Effect of interleukin-1beta and tumor necrosis factor-alpha on gene expression in human endothelial cells[J]. Am J Physiol Cell Physiol, 2003, 284(6):C1577-C1583.
8. Satterthwaite G, Francis SE, Suvarna K, et al. Differential gene expression in coronary arteries from patients presenting with ischemic heart disease:further evidence for the inflammatory basis of atherosclerosis[J]. Am Heart J, 2005, 150(3):488-499.
9. Kiechl S,Willeit J. The nature course of atherosclerosis partⅡ:vascular remodeling[J]. Arterioscler Thromb Vasc Biol, l999, 19(5):l49l-1498.
10. Shiffman D, Mikita T, Tai JT, et al. Large scale gene expression analysis of cholesterol-loaded macrophages[J]. J Biol Chem, 2000, 275(48):37324-37332.
11. 卢次勇, 凌文华, 马静, 等. 氧化型低密度脂蛋白诱导血管内皮细胞基因表达谱的改变[J]. 中国动脉硬化杂志, 2002, 10(6):483-486.
12. 顾菲菲, 高炜, 蒋捷, 等. 基因芯片在同型半胱氨酸诱导动脉粥样硬化基因表达谱变化中的应用[J]. 中国动脉硬化杂志, 2004, 12(4):433-437.
13. Li H, Lewis A, Brodsky S, et al. Homocysteine induces 3-hydroxy-3-methylglutaryl coenzyme a reductase in vascular endothelial cells:a mechanism for development of atherosclerosis?[J]. Circulation, 2002, 105(9):1037-1043.
14. Katsuda S, Kaji T. Atherosclerosis and extracellular matrix[J]. J Atheroscler Thromb, 2003, 10(5):267-274.
15. Vivanco F, Martín-Ventura JL, Duran MC, et al. Quest for novel cardiovascular biomarkers by proteomic analysis[J]. J Proteome Res, 2005, 4(4):1181-1191.
16. Bengtsson E, To F, Grubb A, et al. Absence of the protease inhibitor cystatin C in inflammatory cells results in larger plaque area in plaque regression of apoE-deficient mice[J]. Atherosclerosis, 2005, 180(1):45-53.

West China Medical Journal

Gene Chip Analysis for Artery of Rats with Atherosclerosis

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