AIM:To investigate the effect of AngiotensinⅡ(AngⅡ)on renal tubular Epithelial-Mesenchymal transition,evaluate the relationship between AngⅡand transforming growth factor-β1(TGF-β1)and discussion the mechanism of AngⅡinvolved in tubulointerstitial fibrosis.METHODS:Taking Human proximal tubular epithelial HKC cells as research object.They was maintained in DMEM/F12 medium supplemented with 10%newborn calf serum.Using western blot,etc to testα-SMA,E-cadherin and FN triggered by AngⅡ(10-9,10-8,10-7,10-6mol/L) and the combination of TGF-β1.Using gelatin zymogramphy to study the changes of MMP-2,MMP-9 in supernatant.Using boyden chamber to assay the migration of HKC.RESULTS:1)In HKC induced by AngⅡonly,the expression ofα-SMA and E-cadherin proteins was no change,while FN was highly expressed. 2)α-SMA,E-cadherin and FN triggered by combination of TGF-β1 and AngⅡwas up-regulated,AngⅡcould enhance the effect of TGF-β1.3) AngⅡup-regulated MMP-2,MMP-9 expression of HKC.4)AngⅡ(10-7, 10-6mol/L)could increase the number of cells that migrated across the filter and attached to the underside of boyden chamber.CONCLUSION:1)AngⅡwas involved in EMT,while it was not the critical factor of EMT.2)AngⅡcooperated with TGF-β1 was involved in EMT and may aggravate tubulointerstitial fibrosis. |