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PTEN Inhibits High Glucose‐Induced Phenotypic Transition in Podocytes
Author(s) -
Xing Lingling,
Liu Qingjuan,
Fu Shuxia,
Li Shaomei,
Yang Lin,
Liu Shuxia,
Hao Jun,
Yu Lianying,
Duan Huijun
Publication year - 2015
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25136
Subject(s) - pten , nephrin , podocyte , podocalyxin , pi3k/akt/mtor pathway , protein kinase b , ly294002 , epithelial–mesenchymal transition , tensin , cancer research , microbiology and biotechnology , biology , chemistry , transition (genetics) , signal transduction , endocrinology , biochemistry , kidney , gene , proteinuria
Accumulating evidence has suggested that podocytes undergo epithelial–mesenchymal transition (EMT) in diabetic nephropathy (DN). However, the underlying mechanisms of EMT in podocyte are not well understood. PI3K/Akt pathway is involved in the progression of DN. In the present study, we demonstrated that PI3K/Akt pathway was activated in podocytes exposed to high glucose conditions, accompanied by down‐regulation of the podocalyxin (PCX) and nephrin expression and up‐regulation of the desmin and α‐smooth muscle actin (α‐SMA) expression. Inhibition of PI3K/Akt pathway by chemical LY294002 or Phosphase and tensin homology deleted on chromosome ten (PTEN) prevented the phenotypic transition. These findings indicate that PTEN/PI3K/Akt pathway mediates high glucose‐induced phenotypic transition in podocytes. J. Cell. Biochem. 116: 1776–1784, 2015. © 2015 Wiley Periodicals, Inc.