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.

In this study, we prepared low-molecular-weight hyaluronic acid (LMWHA) powder by γ-irradiation. The chemical and physical properties of γ-irradiated LMWHA and the in vitro cellular growth experiments with γ-irradiated LMWHA were analyzed. Then, hyaluronic acid exposed to 20 kGy of γ-irradiation was used to fabricate a carboxymethyl cellulose (CMC)/LMWHA fabric for wound dressing. Our results showed that γ-irradiated LMWHA demonstrated a significant alteration in carbon–oxygen double bonding and can be detected using nuclear magnetic resonance and ultraviolet (UV)-visible (Vis) spectra. The γ-irradiated LMWHA exhibited strain rate-dependent Newton/non-Newton fluid biphasic viscosity. The viability of L929 skin fibroblasts improved upon co-culture with γ-irradiated LMWHA. In the in vivo animal experiments, skin wounds covered with dressings prepared by γ-irradiation revealed acceleration of wound healing after two days of healing. The results suggest that γ-irradiated LMWHA could be a potential source for the promotion of skin wound healing.

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0.4-T SMF enhanced DPSC migration and dentinogenesis through the activation of the p38 MAPK-related pathway.