Open AccessSuppressive Effect of Taurine on Platelet-Derived Growth Factor (PDGF) BB-Induced c-fos and c-jun mRNA Expressions through Extracellular Signal-Regulated Kinase (ERK) in Mesenchymal Cell Lines
Author(s) -
Masaharu Terashima,
Toshifumi Mitani,
Yu Hosokawa,
Yoshiki Nariai,
Keisuke Imada,
Emiko Kageyama,
Yoshinobu Tanigawa
Publication year - 2003
Publication title -
journal of nutritional science and vitaminology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 56
eISSN - 1881-7742
pISSN - 0301-4800
DOI - 10.3177/jnsv.49.187
Subject(s) - platelet derived growth factor receptor , mapk/erk pathway , signal transduction , microbiology and biotechnology , tyrosine phosphorylation , receptor tyrosine kinase , phosphorylation , platelet derived growth factor , kinase , taurine , biology , mitogen activated protein kinase , chemistry , endocrinology , growth factor , biochemistry , receptor , amino acid
Platelet-derived growth factor (PDGF) plays an important role in the pathogenic course of atherosclerosis, pulmonary fibrosis, and glomerulonephritis, and increased activity of the PDGF signaling pathway has been implicated as a contributing factor in the progression of the diseases. Taurine may be a prophylactic amino acid for atherosclerosis not only by decreasing plasma cholesterol level, but also by inhibiting the cell proliferation-signaling pathway. To elucidate how taurine affects the signaling pathway, we investigated the effect of taurine on the expression of immediate-early genes and activation of mitogen-activated protein kinases (MAPKs) in NIH/3T3 cells as standard mesenchymal cells. Taurine inhibited PDGF-BB-induced c-fos and c-jun mRNA expressions dose-dependently, although structural analogues of taurine did not. Taurine decreased the PDGF-induced p44/p42 ERK (extracellular signal-regulated kinase) phosphorylation state dose-dependently, although no phosphorylation was observed on JNK/SAPK (c-Jun N-terminal kinase/stress-activated protein kinase) and p38 MAPK. Further, PDGF-BB-induced tyrosine phosphorylation of the PDGF-beta receptor was not influenced by treatment with taurine, indicating that taurine never affects ligand-receptor interaction, and may act downstream of the PDGF receptor. Thus, the inhibitory mechanism of taurine on PDGF-induced c-fos and c-jun mRNA expressions may depend on the p44/p42 ERK pathway, but not on PDGF-beta receptor tyrosine phosphorylation, JNK/SAPK or p38 MAPK pathway. These results suggest that taurine may suppress the cell proliferation-signaling pathway through the inhibition of ERK activity and immediate-early gene expression.