Objectives: Neurotrophin-4 (NT-4) is one of the nerotrophic factors, expressing in dental epithelium. Neurotrophin receptor Trks signaling were regulated by cell surface glycosphingolipids (GSLs). Further, the expression pattern of GSLs was dramatically changed during ameloblast differentiation. However, the role of NT-4 and GSLs in tooth development has never been clearly understood. Here, we analyzed the GSLs composition and regulation of NT-4 signaling in dental epithelial (DE) cells. Methods: Expression profile of GSLs in dental epithelium was analyzed by thin layer chromatography (TLC). RT-PCR was performed to determine the expression of NT-4 and their receptor TrkB, and tooth specific markers. ERK1/2 phosphorylation was analyzed by western immunoblotting. Results: NT-4 was expressed in DE cells. Full length of TrkB was not found in DE cells. However, truncated form of TrkB (TrkB-T1) and p75, low affinity of neurotrophin receptor, were highly expressed in DE cells. TLC analysis showed that LacCer, GM3 and Gb4 were the major glycosphingolipids in DE cells. NT-4 treatment induced the phosphorylation of ERK1/2 in DE cells. Increased tyrosine phosphorylation of ERK1/2 was found in the cells treated with exogenous GM3 or LacCer. Further, NT-4 induced the expression of ameloblastin, enamelin and DSPP. Those expressions were enhanced by the exogenous administration of GM3 and LacCer. Conclusion: NT-4, and their receptor TrkB-T1 and p75 were highly expressed in DE cells. GM3 and LacCer enhanced the phosphorylation of ERKs induced by NT-4. These results suggest that NT-4 may cooperate with GSLs on cell surface and regulate the ameloblast differentiation.

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