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Use of 0.4‐Tesla static magnetic field to promote reparative dentine formation of dental pulp stem cells through activation of p38 MAPK signalling pathway
Author(s) -
Lew W.Z.,
Feng S.W.,
Lin C.T.,
Huang H.M.
Publication year - 2019
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.12962
Subject(s) - dental pulp stem cells , pulp (tooth) , in vitro , dentinogenesis , hedgehog signaling pathway , p38 mitogen activated protein kinases , chemistry , dentistry , medicine , microbiology and biotechnology , mapk/erk pathway , biology , biochemistry , odontoblast , signal transduction
Aim To investigate whether static magnetic fields ( SMF s) have a positive effect on the migration and dentinogenesis of dental pulp stem cells ( DPSC s) to promote reparative dentine formation. Methodology In vitro scratch assays and a traumatic pulp exposure model were performed to evaluate the effect of 0.4‐Tesla (T) SMF on DPSC migration. The cytoskeletons of the DPSC s were identified by fluorescence immunostaining and compared with those of a sham‐exposed group. Dentinogenic evaluation was performed by analysing the expressions of DMP ‐1 and DSPP marker genes using a quantitative real‐time polymerase chain reaction ( qRT ‐ PCR ) process. Furthermore, the formation of calcified deposits was examined by staining the dentinogenic DPSC s with Alizarin Red S dye. Finally, the role played by the p38 MAPK signalling pathway in the migration and dentinogenesis of DPSC s under 0.4‐T SMF was investigated by incorporating p38 inhibitor ( SB 203580) into the in vitro DPSC experiments. The Student's t ‐test and the Kruskal–Wallis test followed by Dunn's post ho c test with a significance level of P < 0.05 were used for statistical analysis. Results The scratch assay results revealed that the application of 0.4‐T SMF enhanced DPSC s migration towards the scratch wound ( P < 0.05). The cytoskeletons of the SMF ‐treated DPSC s were found to be aligned perpendicular to the scratch wound. After 20 days of culture, the SMF ‐treated group had a greater number of out‐grown cells than the sham‐exposed group (nonmagnetized control). For the SMF ‐treated group, the DMP ‐1 ( P < 0.05) and DSPP genes ( P < 0.05), analysed by qRT ‐ PCR , exhibited a higher expression. The distribution of calcified nodules was also found to be denser in the SMF ‐treated group when stained with Alizarin Red S dye ( P < 0.05). Given the incorporation of p38 inhibitor SB 203580 into the DPSC s, cell migration and dentinogenesis were suppressed. No difference was found between the SMF ‐treated and sham‐exposed cells ( P > 0.05). Conclusion 0.4‐T SMF enhanced DPSC migration and dentinogenesis through the activation of the p38 MAPK ‐related pathway.