Transforming growth factor-beta1 (TGF-beta1) 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-beta1-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-beta1 (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-beta1-mediated induction of NGF. In addition, SB225002, a G-protein-coupled receptor antagonist, and staurosporine, a serine-threonine kinase inhibitor, partially inhibited TGF-beta1-mediated induction of NGF. Phospho-p38 MAPK was suppressed by SB225002, whereas phospho-JNK was inhibited by staurosporine. We conclude that TGF-beta1 up-regulates NGF in human dental pulp cells. This suggests that TGF-beta1 plays a role in NGF regulation during pulp tissue repair. The signal of TGF-beta1 involves the activation of MAPK, especially p38 and JNK. We suggest that crosstalk between TGF-beta1 and G-protein-coupled receptor signaling also participates in the inductive mechanism.
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