Interleukin-18-induced transdifferentiation in renal proximal tubular cells is mediated by activation of p38MAPK pathway.
- Author:
Jun-feng ZHANG
1
;
Cui-wei YAO
;
Hua-feng LIU
;
Dong LIANG
;
Xiao-wen CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Cell Transdifferentiation; drug effects; Enzyme Inhibitors; pharmacology; Epithelial Cells; cytology; Fibrosis; physiopathology; Humans; Imidazoles; pharmacology; Interleukin-18; pharmacology; Kidney; pathology; Kidney Tubules, Proximal; cytology; MAP Kinase Signaling System; Myofibroblasts; cytology; Pyridines; pharmacology; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Chinese Journal of Applied Physiology 2010;26(2):199-201
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of p38MAPK signaling pathway in interleukin-18-induced transdifferentiation in renal proximal tubular cells.
METHODSHuman proximal tubular epithelial cell line (HK-2 cells) was cultured in vitro. After preincubated with SB203580 (0, 5, 10, 20 micromol/L) for 30 minutes, cells were exposed to IL-18 (100 ng/ml) for 24, 48 and 72 hours respectively. The expressions of a-smooth actin (alpha-SMA) in cultured HK-2 cells were assessed by RT-PCR and ELISA.
RESULTSIL-18-induced expressions of a-SMA mRNA and protein were inhibited obviously by a dose-dependent manner when HK-2 cells were incubated with SB203580 (0, 5, 10, 20 micromol/L) and IL-18 (100 ng/ml) for different time (P < 0.05).
CONCLUSIONIL-18-induced transdifferentiation of renal tubular epithelial cells (RTECs) is suppressed obviously by blocking p38MAPK signaling pathways. IL-18-induced transdifferentiation of RTECs is probably mediated, at least in part, through the activation of p38MAPK signaling pathways.
