PTEN Inhibits High Glucose-Induced Phenotypic Transition in Podocytes.
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.
Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei, 050017, China.|Department of Nephrology, the Second Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Lingling
L
Xing
Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei, 050017, China.
Qingjuan
Q
Liu
Department of Nephrology, the Second Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Shuxia
S
Fu
Department of Nephrology, the Second Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Shaomei
S
Li
Department of Nephrology, the Second Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Lin
L
Yang
Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei, 050017, China.
Shuxia
S
Liu
Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei, 050017, China.
Jun
J
Hao
Department of Nephrology, the Second Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Lianying
L
Yu
Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province, Shijiazhuang, Hebei, 050017, China.
Huijun
H
Duan
D000818:Animals; D002867:Chromones / Q000494:pharmacology; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology*; D051379:Mice; D009025:Morpholines / Q000494:pharmacology; D051059:PTEN Phosphohydrolase / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D050199:Podocytes / Q000187:drug effects* / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*
D002867:Chromones; D009025:Morpholines; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase; C487757:Pten protein, mouse; D005947:Glucose
HIGH GLUCOSE; PHENOTYPIC TRANSITION; PODOCYTES; PTEN