Role of MAPK/JNK signaling pathway on the regulation of biological behaviors of MC3T3‑E1 osteoblasts under titanium ion exposure
- Wen‑Qing Zhu
- Pan‑Pan Ming
- Song‑Mei Zhang
- Jing Qiu
Affiliations: Department of Oral Implantology, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Department of Stomatology, Sir Run Run Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Department of General Dentistry, Eastman Institute for Oral Health, University of Rochester, Rochester, NY 14620, USA
- Published online on: October 11, 2020 https://doi.org/10.3892/mmr.2020.11575
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The oral cavity is a complex environment that is constantly undergoing remodeling. This provides a favorable electrolytic aqueous condition, which causes the corrosion of titanium implants and the release of titanium (Ti) ions. The accumulation of Ti ions in the peri‑implant tissues may affect the osteogenesis process. Therefore, the present study aimed to investigate the possible effects of Ti ions on osteoblast physiology and its underlying mechanism, specifically the MAPK/JNK signaling pathway. In the present study, MC3T3‑E1 osteoblasts were cultured the medium containing 10 ppm Ti ions. Confocal laser scanning microscopy was used to analyze cell morphology and adhesion. Alkaline phosphatase (ALP) activity assay and western blotting were performed to evaluate the expression of proteins associated with osteogenesis such as Runx2 and Osterix. Nuclear translocation of JNK, a key factor of the MAPK signaling pathway, was visualized and analyzed using immunofluorescence staining. The results showed that 10 ppm Ti ions exerted negative effects on the biological behaviors of MC3T3‑E1 cells, which exhibited reduced adhesion, ALP activity and osteogenic differentiation. It was also found that 10 ppm Ti ions activated the MAPK/JNK signaling pathway by promoting the nuclear translocation of JNK via phosphorylation. In addition, the inhibitory effects of 10 ppm Ti ions on MC3T3‑E1 cells was found to be reversed by the JNK inhibitor SP600125. In conclusion, the preset study suggests that the MAPK/JNK signaling pathway serves a key role in the molecular mechanism underlying the changes in osteoblast behavior following Ti ion exposure. These findings may serve as a valuable reference point for the further in‑depth exploration of peri‑implant bone loss.