p38 MAPK mediates high glucose-induced renal tubular epithelial-mesenchymal transition.

• Published in: Sheng li hsüeh pao Vol. 60; no. 6; p. 759
• Main Authors: Fang, Kai-Yun, Shi, Ming-Juan, Xiao, Ying, Gui, Hua-Zhen, Guo, Bing, Zhang, Guo-Zhong
• Format: Journal Article
• Language: Chinese
• Published: China 25.12.2008
• Subjects: Actins - metabolism; Animals; Blotting, Western; Cadherins - metabolism; Cells, Cultured; Diabetes Mellitus, Experimental - metabolism; Epithelial Cells - cytology; Epithelial Cells - metabolism; Epithelial-Mesenchymal Transition; Glucose - pharmacology; Imidazoles - pharmacology; Insulin - pharmacology; Kidney Tubules - cytology; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors; p38 Mitogen-Activated Protein Kinases - metabolism; Pyridines - pharmacology; Rats; Snail Family Transcription Factors; Transcription Factors - metabolism; Transforming Growth Factor beta1 - metabolism
• ISSN: 0371-0874

The aim of the present study was to investigate the role of p38 MAPK in the renal tubular epithelial-mesenchymal transition (TEMT) induced by high glucose. In in vivo study, the rats were randomly divided into control (C), diabetes mellitus (DM) and insulin-treated DM groups. Immunohistochemical staining and Western blot were employed to determine the expression of p38 MAPK and p-p38 MAPK protein in renal cortex of rats. In in vitro study, primary renal tubular epithelial cells (PTECs) were cultured with normal glucose (5.5 mmol/L), high glucose (20 mmol/L D-glucose), high osmolality (20 mmol/L D-mannitol) and SB202190 (a p38 MAPK inhibitor) plus high glucose respectively for 72 h. The expressions of p38 MAPK, p-p38 MAPK, Snail1, transforming growth factor-beta1 (TGF-beta1), alpha-smooth muscle actin (alpha-SMA) and E-cadherin protein and mRNA were detected by immunocytochemical staining, Western blot and RT-PCR. The p38 MAPK and p-p38 MAPK were specifically upregulated by high glucose in both in vivo and in