title: [Angiotensin-(1-7) inhibits hypoxia-induced renal tubular epithelial-to-mesenchymal transition in rats].
abstract: OBJECTIVE
  To investigate the effect of angiotensin-(1-7) [Ang(1-7)] on the transdifferentiation of normal rat kidney proximal tubular epithelia cells (NRK52E) under hypoxic condition induced by cobaltous chloride (Co) and the underlying mechanism.
  
  
  METHODS
  NRK52E cells were divided into control group, Co group, Co+Ang-(1-7) group and Ang-(1-7) group and cultured for 6 d. Expression levels of hypoxia-inducible factor-1α (HIF-lα) and α-smooth muscle actin (α-SMA) were detected by immunocytochemistry. Immunohistochemistry and Western blotting were used to determine the expression of p-ERK1/2 and ELISA to measure the content of collagen type 1 (Col I) in the culture supernatant.
  
  
  RESULTS
  Compared with the control group, the expressions of HIF-lα, α-SMA, Col Iand p-ERK1/2 in the Co group and the Co+Ang-(1-7) group increased significantly (P<0.05) 6 d later. Compared with the Co group, the expressions of HIF-lα, α-SMA, Col Iand p-ERK1/2 in the Co+Ang-(1-7) group decreased significantly (P<0.05).
  
  
  CONCLUSIONS
  Ang-(1-7) can inhibit Co-induced rats' tubular epithelial-to-mesenchymal transition and reduce the production of extracellular matrix. Inhibition of ERK1/2 pathway may play an important role in this process.
authors.affiliation: Department of Nephrology, Hospital Affiliated to Luzhou Medical College, Luzhou 646000, China. ren.tingting2012@sina.com
authors.forename: Tingting
authors.initials: T
authors.lastname: Ren
authors.forename: Hongyan
authors.initials: H
authors.lastname: He
authors.forename: Xiaolan
authors.initials: X
authors.lastname: Yu
authors.forename: Junming
authors.initials: J
authors.lastname: Fan
authors.forename: Jian
authors.initials: J
authors.lastname: Tan
authors.forename: Jian
authors.initials: J
authors.lastname: Liu
mesh_terms: D000199:Actins / Q000378:metabolism; D000803:Angiotensin I / Q000494:pharmacology*; D000818:Animals; D002460:Cell Line; D003035:Cobalt / Q000494:pharmacology; D024042:Collagen Type I / Q000378:metabolism; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D000860:Hypoxia; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007687:Kidney Tubules, Proximal / Q000187:drug effects* / Q000473:pathology*; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats
chemical_list: D000199:Actins; D000803:Angiotensin I; D003035:Cobalt; D024042:Collagen Type I; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D010446:Peptide Fragments; C498862:Acta2 protein, rat; C018021:cobaltous chloride; C118790:angiotensin I (1-7)