| Autor: |
Yongchaitrakul, Tussanee, Pavasant, Prasit |
| Předmět: |
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| Zdroj: |
European Journal of Oral Sciences; Feb2007, Vol. 115 Issue 1, p57-63, 7p, 6 Graphs |
| Abstrakt: |
Transforming growth factor- β1 (TGF- β1) and nerve growth factor (NGF) have been detected in pulp tissues after injury and are implicated in the differentiation of odontoblast-like cells and in pulp tissue repair. We examined TGF- β1-mediated regulation of NGF and investigated its signaling pathways in human dental pulp cells. Analyses by reverse transcription–polymerase chain reaction (RT–PCR) and enzyme-linked immunosorbent assay (ELISA) revealed that TGF- β1 (1 ng ml−1) induced NGF mRNA and protein expression through the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Blockade of the p38 MAPK and JNK pathways with the respective upstream inhibitors (SB203580 and SP600125) abolished the TGF- β1-mediated induction of NGF. In addition, SB225002, a G-protein-coupled receptor antagonist, and staurosporine, a serine-threonine kinase inhibitor, partially inhibited TGF- β1-mediated induction of NGF. Phospho-p38 MAPK was suppressed by SB225002, whereas phospho-JNK was inhibited by staurosporine. We conclude that TGF- β1 up-regulates NGF in human dental pulp cells. This suggests that TGF- β1 plays a role in NGF regulation during pulp tissue repair. The signal of TGF- β1 involves the activation of MAPK, especially p38 and JNK. We suggest that crosstalk between TGF- β1 and G-protein-coupled receptor signaling also participates in the inductive mechanism. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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