PTEN Inhibits High Glucose-Induced Phenotypic Transition in Podocytes

J Cell Biochem. 2015 Aug;116(8):1776-84. doi: 10.1002/jcb.25136.

Abstract

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.

Keywords: HIGH GLUCOSE; PHENOTYPIC TRANSITION; PODOCYTES; PTEN.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chromones / pharmacology
  • Epithelial-Mesenchymal Transition / drug effects
  • Gene Expression Regulation / drug effects
  • Glucose / pharmacology*
  • Mice
  • Morpholines / pharmacology
  • PTEN Phosphohydrolase / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Podocytes / drug effects*
  • Podocytes / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects*

Substances

  • Chromones
  • Morpholines
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • Pten protein, mouse
  • Glucose