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.