Head & neck · 2011
Thrombin-stimulated connective tissue growth factor (CTGF/CCN2) production in human buccal mucosal fibroblasts: Inhibition by epigallocatechin-3-gallate.
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Chang Jenny Zwei-Chieng, Yang Wan-Hsien, Deng Yi-Ting, Chen Hsin-Ming, Kuo Mark Yen-Ping
Аннотация
BACKGROUND: Connective tissue growth factor (CTGF/CCN2) is associated with many human fibrotic disorders and was found to overexpress in oral submucous fibrosis (OSF). OSF is the result of persistent chemical irritation and microtrauma to oral mucosa from areca nut. Microtrauma could lead to the release of thrombin.
METHODS: Thrombin-induced CCN2 expression and its signaling pathways were assessed by Western blot analyses in human buccal mucosal fibroblasts.
RESULTS: Thrombin stimulated CCN2 synthesis in buccal mucosal fibroblasts via activation of protease-activated receptor-1. Pretreatment with antioxidant N-acetyl-L-cysteine, apoptosis signal-regulating kinase 1 inhibitor thioredoxin, and c-Jun NH(2) -terminal kinase inhibitor SP600125 significantly reduced thrombin-induced CCN2 synthesis. Epigallocatechin-3-gallate completely inhibited thrombin-induced CCN2 synthesis.
CONCLUSION: Thrombin produced by microtrauma may contribute to the pathogenesis of OSF by up-regulating CCN2 expression. This effect could be mediated by protease-activated receptor-1, reactive oxygen species, apoptosis signal-regulating kinase 1, and c-Jun NH(2) -terminal kinase pathways and prevented by epigallocatechin-3-gallate.
METHODS: Thrombin-induced CCN2 expression and its signaling pathways were assessed by Western blot analyses in human buccal mucosal fibroblasts.
RESULTS: Thrombin stimulated CCN2 synthesis in buccal mucosal fibroblasts via activation of protease-activated receptor-1. Pretreatment with antioxidant N-acetyl-L-cysteine, apoptosis signal-regulating kinase 1 inhibitor thioredoxin, and c-Jun NH(2) -terminal kinase inhibitor SP600125 significantly reduced thrombin-induced CCN2 synthesis. Epigallocatechin-3-gallate completely inhibited thrombin-induced CCN2 synthesis.
CONCLUSION: Thrombin produced by microtrauma may contribute to the pathogenesis of OSF by up-regulating CCN2 expression. This effect could be mediated by protease-activated receptor-1, reactive oxygen species, apoptosis signal-regulating kinase 1, and c-Jun NH(2) -terminal kinase pathways and prevented by epigallocatechin-3-gallate.
Предметные рубрики MeSH
Amino Acid Chloromethyl KetonesAnticarcinogenic AgentsArecaBlotting, WesternCatechinCells, CulturedConnective Tissue Growth FactorFibroblastsHemostaticsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5MasticationMouth MucosaOral Submucous FibrosisReactive Oxygen SpeciesReceptor, PAR-1Serine Proteinase InhibitorsThrombinUp-Regulation