文章摘要
高 雯,狄 佳,闻 萍,江 蕾,熊明霞,杨俊伟.血管紧张素Ⅱ参与肾小管上皮细胞转分化的实验研究[J].南京医科大学学报,2009,29(5):623~627
血管紧张素Ⅱ参与肾小管上皮细胞转分化的实验研究
Experimental study of angiotensinⅡ(AngⅡ) involved in renal epithelial-mesenchymal transition
  
DOI:10.7655
中文关键词: 血管紧张素Ⅱ  转化生长因子-β1  转分化  纤维化
英文关键词: angiotensin Ⅱ  TGF-β1  EMT  fibrosis
基金项目:国家自然科学基金资助(30470800,30771010);科技部“973”重点项目(2006CB503909);国家人事部回国人员科研启动基金;江苏省“六大人才”高峰项目;江苏省“科教兴卫”工程医学领军人才项目
作者单位
高 雯 南京医科大学第一附属医院肾内科,江苏 南京 210029 
狄 佳 南京医科大学第一附属医院肾内科,江苏 南京 210029 
闻 萍 南京医科大学第一附属医院肾内科,江苏 南京 210029 
江 蕾 南京医科大学第一附属医院肾内科,江苏 南京 210029 
熊明霞 南京医科大学第一附属医院肾内科,江苏 南京 210029 
杨俊伟 南京医科大学第二附属医院肾内科,江苏 南京 210003 
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中文摘要:
      目的:本文通过观察血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)影响肾小管上皮细胞转分化(epithelial-mesenchymal transition,EMT)的作用,以及和转化生长因子-?茁1(transforming growth factor,TGF-?茁1)作用的关系,探讨AngⅡ参与肾小管间质纤维化的作用机制?方法:以人肾小管上皮细胞株(human kidney cell)HKC细胞为研究对象,采用蛋白印迹等方法,观察AngⅡ(10-9?10-8?10-7?10-6 mol/L),及其与TGF-?茁1共同作用对该细胞表达?琢-平滑肌肌动蛋白(?琢-smooth muscle actin,?琢-SMA)?E-钙黏蛋白(E-cadherin)和纤维连接蛋白(fibronectin,FN)的影响?明胶酶谱法检测细胞培养上清液中基质金属蛋白酶-2和基质金属蛋白酶-9(MMP-2和MMP-9)的变化,Boyden小室检测HKC细胞的迁移能力?结果:①单独应用Ang Ⅱ不能够造成HKC细胞E-cadherin表达的变化,也不能诱导?琢-SMA表达,但是却能上调FN的表达;②与TGF-?茁1共同作用时能够加强TGF-?茁1影响E-cadherin,?琢-SMA和FN表达的作用;③AngⅡ能够增加HKC生成MMP-2和MMP-9;④AngⅡ能够(10-7和10-6 mol/L)增加HKC细胞迁移至Boyden小室膜下侧面的数目?结论:①AngⅡ可以参与EMT过程,但不是导致EMT的关键因素;②Ang Ⅱ能够以协同的方式参与TGF-?茁1导致的EMT,可能以此方式加重肾小管间质的纤维化?
英文摘要:
      Objective:To investigate the effect of Angiotensin Ⅱ(AngⅡ)on renal tubular Epithelial-Mesenchymal transition,evaluate the relationship between AngⅡ and transforming growth factor-β1(TGF-β1) and discuss the mechanism of AngⅡ involved in tubulointerstitial fibrosis. Methods:Human proximal tubular epithelial HKC cells were taken as research objects. They was maintained in DMEM/F12 medium supplemented with 10% newborn calf serum. α-SMA,E-cadherin and FN triggered by AngⅡ(10-9,10-8, 10-7,10-6 mol/L),and the combination of TGF-β1 were tested by Western blot. The changes of MMP-2 and MMP-9 in supernatant were detected by gelatin zymogramphy. The migration of HKC was assayed by Boyden chamber. Results:①In HKC induced by AngⅡ only,the expression of α-SMA and E-cadherin proteins has no change,while FN was highly expressed. ②α-SMA,E-cadherin and FN triggered by combination of TGF-β1 and AngⅡ was up-regulated,and AngⅡ could enhance the effect of TGF-β1. ③AngⅡ up-regulated MMP-2 and MMP-9 expressions of HKC. ④AngⅡ(10-7,10-6 mol/L) could increase the number of cells that migrated across the filter and attached to the underside of boyden chamber. Conclusion:①Ang Ⅱ was involved in EMT,while it was not the critical factor of EMT. ②AngⅡ cooperated with TGF-β1 was involved in EMT and might aggravate tubulointerstitial fibrosis.
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