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ACE2基因表达增加对人脐静脉内皮细胞增殖、凋亡的影响

The effect of ACE2 gene overexpression on proliferation and apoptosis of human umbilical vein endothelial cells induced by Angiotensin lI
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摘要 目的探索在AngII干预下ACE2基因表达增加对人血管内皮细胞增殖、凋亡的影响。方法原代培养人脐静脉血管内皮细胞。用构建、包装好的慢病毒重组ACE2基因表达载体(Lentiviral—ACE2)以感染复数为10(MOI=10)感染人脐静脉内皮细胞(HUVEC)。感染72h后,以AnglI(终浓度为10。mol/L)干预细胞,倒置相差显微镜观察各组HUVEC的形态学变化,AlamarBlue试剂检测各组HUVEC增殖功能,TUNEL细胞凋亡检测试剂盒检测各组HUVEC的凋亡。结果AngⅡ组与AngII+Lentiviral—GFP组细胞生长状态差,生长缓慢,形态不规则并且有不同程度脱壁悬浮的细胞;而正常细胞对照组与AngII+Lentiviral—ACE2组细胞生长状态良好,圆形、卵圆形,饱满,形态正常呈“铺路石”样生长,紧密贴壁,悬浮细胞少。AngII组较正常细胞对照组、Ang1I+Lentiviral—ACE2组AlamarBlue被还原率明显降低(P〈O.05)。Ang11组的凋亡指数为(0.1165±0.0181),与正常细胞对照组凋亡指数(0.0373±0.0113)和AngⅡ+Lentiviral—ACE2组凋亡指数(0.0540±0.0061)相比差异有统计学意义(P〈0.05)。AngII组与AngⅡ+Lentiviral—GFP相比、正常细胞对照组与AngII+Lentiviral—ACE2组相比,AlamarBlue被还原率和凋亡指数差异无统计学意义。结论AngⅡ具有促进人脐静脉内皮细胞增殖能力下降和凋亡增加的作用。ACE2表达增~IIII抑制AngⅡ诱导的人脐静脉内皮细朐增殖活件降低和凋亡增加.对人脐静脉内皮细胞具有保护作用。 Objective To study the effect of ACE2 gene overexpression on proliferation and apoptosis in- duced by angiotensin H in human umbilical vein endothelial cells. Methods Human umbilical endothelial cells were cultured in vitro. The human umbilical vein endothelial cells were infected by recombinant ACE2 gene lentiviral vector (Lentiviral-ACE2) with multiplicity of infection of 10 (MOI=IO) which had been constructed, packaged. After infected by Lentiviral-ACE2 72 hours. The human umbilical vein endothelial cells were treated with Ang II (at final concentration 10-7 mol/L). The morphological changes of human umbilical vein endothelial cells in each group was observed by inverted phase contrast microscope. The proliferation function of each group human umbilical vein endothelial cells was detected by AlamarBlue reagents. The apoptosis in each group human umbilical vein endothelial cells was researched by TUNEL Apoptosis Detection Kit. Results The cell growth state in Ang !1 group and Ang !1 + Lentiviral-GFP group were poor, slow growth, irregular shape and there were some degrees of cell suspension off wall, while the normal cell control group and group of Ang I1 +Lentiviral-ACE2 cell growth were in good condition, round, oval, full, and they were "paving stone"-like normal morphology growth and closely adherent, having little suspension cells. Ang I1 group' AlamarBlue reduction rate was significantly lower (P〈0.05) than those of normal cell control group and Ang Ill +Lentiviral-ACE2 group. The apoptosis indexwas also a statistical significance (P〈0.05) in Ang ]I group (0.1165±0.0181) compared to normal cell control group(0.0373±0.0113) and Ang l] +Lentiviral-ACE2 group (0.0540±0.0061). The AlamarBlue reduction rate and apoptosis index between Ang II group and Ang II +Lentiviral-GFP was not statistically significant, nor between normal cells control group and Ang lI +Lentiviral-ACE2. Conclusion Ang 11 has a function that it can reduce the proliferation and increase the apoptosis of human umbilical vein endothelial cells,while the overexpression of ACE2 gene can restrain those actions.
出处 《中国心血管病研究》 CAS 2013年第7期540-544,I0004,共6页 Chinese Journal of Cardiovascular Research
关键词 血管紧张素转化酶2 人脐静脉内皮细胞 增殖 凋亡 Angiotensin-converting enzyme 2 Human umbilical vein endothelial cells Proliferation Apoptosis
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参考文献19

  • 1Schmidt-Ott KM, Kagiyama S, Phillips MI. The multiple actions of angiotensin in atherosclerosis. Regul Pept,2009,93:65-67.
  • 2Wassmann S, Nickenig G. Pathophysiological regulation of the AT-receptor and implications for vascular disease. J Hypertens, 2006,24 : S15-$21.
  • 3王前胜,晋学庆,卢卓强.慢病毒重组ACE2基因表达载体的构建及其感染人脐静脉内皮细胞的研究[J].中国心血管病研究,2010,8(3):214-217. 被引量:2
  • 4盛大平,徐元宏.alamarBlue在临床检验中的应用[J].国外医学(临床生物化学与检验学分册),2005,26(6):367-368. 被引量:13
  • 5A1-Nasiry S, Geusens N, Hanssens M, et al. The use of Alamar Blue assay for quantitative analysis of viability, migration and in- vasion of choriocarcinoma ceils. Human Reproduction,2007,22: 1304-1309.
  • 6Cline DB, Polak ES, Buck CA, et al. Endothelial cells in physi- ology and in the pathophysiology of vascular disorders. Blood, 1998,91 : 3527-3561.
  • 7Ckoy JC, Granville DJ, Hunt DW, et al. Endothelial cell apop- toais:biochemical characteristics and potential implications for atherosclerosis. J Mol cell cardiol, 2001,33:1673-1690.
  • 8刘慧青,张岫美,魏欣冰.氯沙坦对血管紧张素II致培养的牛脑微血管内皮细胞损伤的保护作用[J].药学学报,2003,38(1):5-9. 被引量:15
  • 9Dimmeler S, Rippmann V, Weiland U, et al. Angiotensin I1 in- duces apoptosis of human endothelial cells. Protective effect ofnitric oxide. Cir Res, 1997,81 : 970-976.
  • 10He M, He X, Xie Q, et al. Angiotensin ]I induces the expres- sion of tissue factor and its mechanism in human monocytes. Thromb Res, 2006, 117 : 579-590.

二级参考文献37

  • 1王前胜,晋学庆.ACE2-Ang-(1-7)-Mas轴及其基因学研究进展[J].中国心血管病研究,2009,7(10):784-787. 被引量:9
  • 2钟久昌,黄东阳,余细勇.高血压大鼠ACE2的表达及其与一氧化氮相关性分析[J].高血压杂志,2005,13(9):564-567. 被引量:10
  • 3黄群英,晋学庆,吴可贵,翁智远,许昌声,王华军.自发性高血压大鼠肾脏血管紧张素转换酶2 mRNA转录及其蛋白表达[J].中华高血压杂志,2007,15(6):473-476. 被引量:10
  • 4Donoghue M, Hsieh F, Baronas E, et al. A novel angiotensin-convetting enzyme-related earboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9. Cire Res, 2000,87 : E1-9.
  • 5Tipnis SR, Hooper NM, Hyde R,et al. A human homolog of angiotensin-converting enzyme. Cloning and functional expression as a captopfil-insensitive carboxypeptidase. J Biol Chem, 2000,275: 33238-33243.
  • 6Raizada MK, Der Sarkissian S. Potential of gene therapy strategy for the treatment of hypertension. Hypertension, 2006,47 : 6-9.
  • 7Oudit GY,Crackower MA,Baekx PH,et al. The role of ACE2 in cardiovascular physiology. Trends Cardiovac Med, 2003,13 : 93 - 101.
  • 8Turner A J, Hooper NM. The angiotension-converting enzyme gene family : genomics and pharmacology.Trends Phannacol Sci, 2002, 23 : 177-183.
  • 9Miyoshi H,Takabashi M, Gage FH, et al. Stable and eficient gene transfer into the retina using an HIV-based lentiviral vector. Prec Nail Acad Sci USA, 1997,94:10319-10323.
  • 10Goldman MJ,Lee PS,Yang JS,et al. Lentiviral vectors for gene therapy of cystic fibrosis. Hum Gene Ther, 1997,8 : 2261-2268.

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