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suck abstract from ncbi


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pmid23746243      Xi+Bao+Yu+Fen+Zi+Mian+Yi+Xue+Za+Zhi 2013 ; 29 (6): 593-6
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  • Angiotensin-(1-7) inhibits hypoxia-induced renal tubular epithelial-to-mesenchymal transition in rats #MMPMID23746243
  • Ren T; He H; Yu X; Fan J; Tan J; Liu J
  • Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2013[Jun]; 29 (6): 593-6 PMID23746243show ga
  • 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-1alpha (HIF-lalpha) and alpha-smooth muscle actin (alpha-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-lalpha, alpha-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-lalpha, alpha-SMA, Col Iand p-ERK1/2 in the Co+Ang-(1-7) group decreased significantly (P<0.05). CONCLUSION: 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.
  • |*Hypoxia[MESH]
  • |Actins/metabolism[MESH]
  • |Angiotensin I/*pharmacology[MESH]
  • |Animals[MESH]
  • |Cell Line[MESH]
  • |Cobalt/pharmacology[MESH]
  • |Collagen Type I/metabolism[MESH]
  • |Epithelial-Mesenchymal Transition/*drug effects[MESH]
  • |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH]
  • |Kidney Tubules, Proximal/*drug effects/*pathology[MESH]
  • |Mitogen-Activated Protein Kinase 1/metabolism[MESH]
  • |Mitogen-Activated Protein Kinase 3/metabolism[MESH]
  • |Peptide Fragments/*pharmacology[MESH]


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