title: [Role of integrin-linked kinase in renal tubular epithelial-mesenchymal transition of mice with obstructive nephropathy].
abstract: OBJECTIVE
  To investigate the expression of integrin-linked kinase (ILK) in kidneys of mice with unilateral ureteral obstruction and its relevance with the epithelial-mesenchymal transition.
  
  
  METHODS
  Mice were randomly divided into two groups, sham operation (C, n = 20) and unilateral ureteral obstruction (UUO, n = 40). The animals were sacrificed at day 1, 3, 7 and 14 respectively after the surgery. Tubulointerstitial fibrosis (TIF) was graded according to Masson staining. The protein level of ILK was examined by Western blot. Tissue/cytological expression for ILK, alpha-SMA and E-cadherin were investigated by immunohistochemistry. The mRNA levels of ILK, alpha-SMA and E-cadherin were analyzed by quantitative real-time PCR.
  
  
  RESULTS
  In the control animals (group C), weak staining for ILK was detected mainly in the podocytes. Significant increase of staining for ILK in the experimental mice (UUO group) was detected from day 1 onward (t = 16.5, P < 0.01), reaching the peak at day 7. The protein expression of E-cadherin was continuously down-regulated from day 3 onward after surgery (t = 21.0, P < 0.01), while expression for alpha-SMA was up-regulated. From day 1 to day 7, the protein expression of ILK was positively correlated with alpha-SMA (R = 0.88, P < 0.01), but negatively correlated with E-cadherin (R = -0.87, P < 0.01). The mRNA expression of ILK and alpha-SMA analyzed by real-time PCR increased from postoperative day 1 and 3 respectively, but the mRNA expression of E-cadherin decreased from day 3 onward.
  
  
  CONCLUSIONS
  Increasing expression of ILK occurs in the early phase of UUO mouse and may play an important role in the process of TIF through mediating the epithelial-mesenchymal transition.
authors: Institute of Nephrology, Zhong Da Hospital, Southeast University, Nanjing 210009, China.
authors: Hui-ling
authors: HL
authors: Xia
authors: Bi-cheng
authors: BC
authors: Liu
authors: Xiao-liang
authors: XL
authors: Zhang
authors: Dian-ge
authors: DG
authors: Liu
authors: Ji-ning
authors: JN
authors: Wu
authors: Jian-dong
authors: JD
authors: Zhang
authors: Yu-xiang
authors: YX
authors: Gong
mesh_terms: D000199:Actins / Q000096:biosynthesis / Q000235:genetics; D000818:Animals; D015153:Blotting, Western; D015820:Cadherins / Q000096:biosynthesis / Q000235:genetics; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D005355:Fibrosis; D007150:Immunohistochemistry; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008648:Mesoderm / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009130:Muscle, Smooth / Q000737:chemistry; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014517:Ureteral Obstruction / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D000099200:Scaffold Protein ILK
chemical_list: D000199:Actins; D015820:Cadherins; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D000099200:Scaffold Protein ILK; C541116:ACTA2 protein, human