Static magnetic field regulates proliferation, migration, and differentiation of human dental pulp stem cells by MAPK pathway

• Published in: Cytotechnology (Dordrecht) Vol. 74; no. 3; pp. 395 - 405
• Main Authors: Na, Jing, Zhang, Lingyu, Zheng, Lisha, Jiang, Jingyi, Shi, Qiusheng, Li, Chiyu, Fan, Yubo
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.06.2022; Springer Nature B.V
• Subjects: Biochemistry; Biomedicine; Biotechnology; c-Jun protein; Cell cycle; Cell growth; Cell migration; Cell proliferation; Cell viability; Chemistry; Chemistry and Materials Science; Dental pulp; Dentistry; Extracellular signal-regulated kinase; JNK protein; Kinases; Magnetic fields; MAP kinase; Medical research; Membranes; Mineralization; Odontogenesis; Original; Original Article; Phosphorylation; Proteins; Stem cells; Transcription factors; Wound healing; St Louis Missouri; United States > US; China; Static magnetic field; MAPK; Osteogenic differentiation; Dental pulp stem cells; Odontogenic differentiation
• ISSN: 0920-9069; 1573-0778
• DOI: 10.1007/s10616-022-00533-3

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.