Static magnetic fields enhance dental pulp stem cell proliferation by activating the p38 mitogen-activated protein kinase pathway as its putative mechanism.

Dental pulp stem cells (DPSCs) can be a potential stem cell resource for clinical cell therapy and tissue engineering. However, obtaining a sufficient number of DPSCs for repairing defects is still an issue in clinical applications. Static magnetic fields (SMFs) enhance the proliferation of several cell types. Whether or not SMFs have a positive effect on DPSC proliferation is unknown. Therefore, the aim of this study was to investigate the effect of SMFs on DPSC proliferation and its possible intracellular mechanism of action. For methodology, isolated DPSCs were cultured with a 0.4-T SMF. Anisotropy of the lipid bilayer was examined using a fluorescence polarization-depolarization assay. The intracellular calcium ions of the SMF-treated cells were analysed using Fura-2 acetoxymethyl ester labelling. The cytoskeletons of exposed and unexposed control cells were labelled with actin fluorescence dyes. Cell viability was checked when the tested cells were cultured with inhibitors of ERK, JNK and p38 to discern the possible signalling cascade involved in the proliferative effect of the SMF on the DPSCs. Our results showed that SMF-treated cells demonstrated a higher proliferation rate and anisotropy value. The intracellular calcium ions were activated by SMFs. In addition, fluorescence microscopy images demonstrated that SMF-treated cells exhibit higher fluorescence intensity of the actin cytoskeletal structure. Cell viability and real-time polymerase chain reaction suggested that the p38 signalling cascade was activated when the DPSCs were exposed to a 0.4-T SMF. F-actin intensity tests showed that SB203580-treated cells decreased even with SMF exposure. Additionally, the F-/G-actin ratio increased due to slowing of the cytoskeleton reorganization by p38 mitogen-activated protein kinase inhibition. According to these results, we suggest that a 0.4-T SMF affected the cellular membranes of the DPSCs and activated intracellular calcium ions. This effect may activate p38 mitogen-activated protein kinase signalling, and thus reorganize the cytoskeleton, which contributes to the increased cell proliferation of the DPSCs.