title: [Effect of chronic enhanced external counterpulastion on gene expression profiles of arterial endothelial cells of pigs fed with high-cholesterol diet].
abstract: OBJECTIVE
  To investigate the effect of chronic enhanced external counterpulastion (EECP) on gene expression profiles of arterial endothelial cells (ECs) of pigs fed with high-cholesterol diet.
  
  
  METHODS
  Eight male pigs were fed with high-cholesterol diet for 12 weeks to induce arteriosclerosis and subjected to EECP for accumulative 36 h (2 h every other day for 18 sessions). Another 8 pigs on cholesterol-enriched diet and 6 normally fed pigs served as the arteriosclerosis model group and normal control group, respectively, and the high-cholesterol diet was maintained until the end of EECP treatment. The coronary artery was then isolated for transmission electro microscopy, and the abdominal aorta was observed using Sudan III staining. The gene expression profiles in ECs from the thoracic aorta using cDNA microarrays.
  
  
  RESULTS
  Macrophages and foam cells were detected beneath the ECs in the coronary artery of pigs in the model group, but not in the other two groups. The ratios of Sudan III-positive area in the celiac aorta were significantly lower in normal control and EECP groups than in the model control group (P<0.05). Compared with the normal control group, the gene expressions of integrins-beta1 and CTGF were up-regulated in the model group. Compared with the model group, the expressions of integrins-beta1, CTGF and VCAM-1 were down-regulated and eNOS up-regulated in EECP group.
  
  
  CONCLUSIONS
  Chronic EECP may reduce endothelial injury, down-regulate the gene expression level of integrin-beta1, CTGF and VCAM-1, lower cholesterol uptake and attenuate arterial endothelial inflammation to protect the pigs fed with high-cholesterol diet from arteriosclerosis.
authors.affiliation: Key Lab of Assisted Circulation of the State Ministry of Public Health, First Affiliated Hospital, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China. hexxhong@163.com
authors.forename: Xiao-hong
authors.initials: XH
authors.lastname: He
authors.forename: Gui-fu
authors.initials: GF
authors.lastname: Wu
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xiao-lin
authors.initials: XL
authors.lastname: Chen
authors.forename: Zhen-sheng
authors.initials: ZS
authors.lastname: Zhang
authors.forename: Cheng-yang
authors.initials: CY
authors.lastname: Zhan
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.forename: Jian-gui
authors.initials: JG
authors.lastname: He
authors.forename: Yan
authors.initials: Y
authors.lastname: Xiong
authors.forename: Dian-qiu
authors.initials: DQ
authors.lastname: Fang
authors.forename: Lu-guang
authors.initials: LG
authors.lastname: Liang
authors.forename: Yue-tao
authors.initials: YT
authors.lastname: Qian
authors.forename: Gui-fang
authors.initials: GF
authors.lastname: Lin
authors.forename: Gang
authors.initials: G
authors.lastname: Dai
authors.forename: Ming-zhe
authors.initials: MZ
authors.lastname: Feng
authors.forename: Kui-jian
authors.initials: KJ
authors.lastname: Wang
authors.forename: Zhen-yu
authors.initials: ZY
authors.lastname: Zhu
authors.forename: Hong
authors.initials: H
authors.lastname: Ma
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism / Q000473:pathology; D001161:Arteriosclerosis / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D015908:Counterpulsation / Q000379:methods*; D004036:Diet, Atherogenic; D042783:Endothelial Cells / Q000378:metabolism*; D020869:Gene Expression Profiling; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D013552:Swine