南方医科大学学报

南方医科大学学报 ›› 2015, Vol. 35 ›› Issue (05): 652-.

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慢病毒介导ACE2过表达对血管紧张素Ⅱ诱导的大鼠肝细胞的白蛋白表达及迁移能力的影响

张莉莉，张文雍，李洋，李旭   

  • 出版日期:2015-05-20 发布日期:2015-05-20

Lentivirus-mediated angiotensin-converting enzyme 2 overexpression inhibits
angiotensin II-induced albumin down-regulation and enhancement of migration in rat
hepatocytes

  • Online:2015-05-20 Published:2015-05-20

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摘要： 目的探讨血管紧张素转换酶2（Angiotensin-converting enzyme 2, ACE2）过表达对血管紧张素Ⅱ（Angiotensin II, Ang
Ⅱ）诱导的肝细胞白蛋白表达下调及细胞迁移性增强的抑制作用。方法常规培养大鼠肝细胞系BRL-3A细胞株，予以Ang II
（10-7 mol/L）进行刺激，观察不同处理时间（24、48 h）组肝细胞内白蛋白、波形蛋白（vimentin）表达及细胞迁移性的改变；通过构
建lentiACE2慢病毒载体，建立稳定过表达ACE2的细胞系，并分别用AngⅡ、A779进行干预，观察肝细胞内相应蛋白表达及其
迁移性的改变。采用细胞免疫荧光、Western blot检测细胞中蛋白水平变化；Transwell迁移实验观察不同处理组细胞迁移能力
的改变。结果AngⅡ处理组肝细胞内vimentin表达显著增加、albumin表达减低，细胞迁移能力显著增强，并具有时间依赖效
应。ACE2 过表达大鼠肝细胞albumin 表达明显升高，vimentin 蛋白表达下降，该作用被MAS受体抑制剂A779 阻断。同时
ACE2过表达显著抑制AngⅡ的作用，vimentin合成显著下降，albumin表达水平显著升高，细胞迁移能力受到抑制。结论ACE2
过表达可抑制AngⅡ诱导的肝细胞albumin表达下调及迁移能力增强。

Abstract: Objective To investigate the inhibitory effect of angiotensin-converting enzyme 2 (ACE2) on angiotensin II (Ang
II)-induced down-regulation of albumin expression and enhancement of cell migration in rat hepatocytes. Methods Cultured
rat hepatocyte were treated with Ang II (10-7 mol/L) for different time lengths, and the protein expressions of vimentin and
albumin and cell migration were detected. The cells transfected with lentiGFP or lentiACE2 were treated with A779 for 1 h and
then with Ang II, and Western blotting and immunofluorescent cytochemistry were used to detect the protein levels; the cell
migration was evaluated by Transwell assay. Result Ang II induced significantly increased vimentin expression and reduced
albumin expression in rat hepatocytes in a time-dependent manner. Overexpression of ACE2 obviously inhibited the
up-regulation of vimentin expression, reduction of albumin expression, and enhancement of cell migration induced by Ang II.
Conclusion ACE2 overexpression can inhibit Ang II-induced up-regulation of vimentin, reduction of albumin expression, and
enhancement of cell migration in rat hepatocytes.