Na Jing, Zhang Lingyu, Zheng Lisha, Jiang Jingyi, Shi Qiusheng, Li Chiyu, Fan Yubo
Key Laboratory of Biomechanics and Mechanobiology (Beihang University), Ministry of Education, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Xue Yuan Road No.37, Haidian District, Beijing, 100083 China.
Cytotechnology. 2022 Jun;74(3):395-405. doi: 10.1007/s10616-022-00533-3. Epub 2022 Apr 20.
Magnetic materials are now commonly used in dental clinics. These materials generally produce a static magnetic field (SMF). While it is known that SMF can affect cells' behaviors such as proliferation, migration, and differentiation, the mechanisms underlying these effects are still unclear. Our study investigates the role of the mitogen-activated protein (MAP) kinase pathway in SMF-induced proliferation, migration, osteogenic/odontogenic differentiation, and mineralization in human dental pulp stem cells (DPSCs). Human DPSCs were exposed to SMF of 1 mT and the phosphorylated MAP kinases were detected by Western blot analysis. Three MAP kinases inhibitors were pre-cultured with DPSCs and exposed to SMF for 24 h. Cell viability was analyzed using Cell Counting Kit-8. Cell migration was tested by a wound healing assay. Osteogenic/odontogenic differentiation was detected by ALP staining assay, ALP and DSPP Western blot analysis. Mineralization was studied by alizarin red staining analysis. SMF activated phosphorylation of c-Jun N-terminal kinase (JNK), P38 and extracellular signal-regulated kinase (ERK). The inhibition of JNK, P38, and ERK signaling decreased SMF-induced proliferation and migration. ERK and P38 play more important roles in SMF-induced ALP staining and protein expression. JNK was vital for SMF-induced DSPP expression. JNK, P38, and ERK all involved in SMF-mediated mineralization. Our study demonstrated that the MAPK pathway regulated SMF-induced proliferation, migration, osteogenic/odontogenic differentiation, and mineralization in human DPSCs.
磁性材料目前在牙科诊所中普遍使用。这些材料通常会产生静磁场（SMF）。虽然已知SMF会影响细胞的增殖、迁移和分化等行为，但其潜在机制仍不清楚。我们的研究调查了丝裂原活化蛋白（MAP）激酶途径在SMF诱导的人牙髓干细胞（DPSC）增殖、迁移、成骨/成牙分化及矿化中的作用。将人DPSC暴露于1 mT的SMF中，并通过蛋白质免疫印迹分析检测磷酸化的MAP激酶。三种MAP激酶抑制剂与DPSC预培养，并暴露于SMF 24小时。使用细胞计数试剂盒-8分析细胞活力。通过伤口愈合试验检测细胞迁移。通过碱性磷酸酶（ALP）染色试验、ALP和牙本质涎磷蛋白（DSPP）蛋白质免疫印迹分析检测成骨/成牙分化。通过茜素红染色分析研究矿化情况。SMF激活了c-Jun氨基末端激酶（JNK）、P38和细胞外信号调节激酶（ERK）的磷酸化。抑制JNK、P38和ERK信号传导可降低SMF诱导的增殖和迁移。ERK和P38在SMF诱导的ALP染色和蛋白质表达中发挥更重要的作用。JNK对SMF诱导的DSPP表达至关重要。JNK、P38和ERK均参与SMF介导的矿化过程。我们的研究表明，MAPK途径调节了SMF诱导的人DPSC增殖、迁移、成骨/成牙分化及矿化。
