Role of MAPK/JNK signaling pathway on the regulation of biological behaviors of MC3T3‑E1 osteoblasts under titanium ion exposure

Abstract

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.

Sitagliptin attenuates Porphyromonas gingivalis virulence and inflammatory response in macrophage on titanium

“…IL-12 is not toxic itself but prompts a neutrophil response that determined the severity of tissue damage [57,58], therefore our results may suggest that sitagliptin can control excessive levels of IL-12. Studies determined the important roles of MAPK and AKT signaling pathways in peri-implantitis [59][60][61]. Our study showed that P. gingivalis LPS significantly enhanced the phosphorylation of p38 MAPK, AKT and ERK while the treatment of sitagliptin decreased the phosphorylation, suggesting that sitagliptin may exert anti-inflammatory effects by inhibiting the MAPK and AKT signaling pathways.…”

Sitagliptin Attenuates Porphyromonas Gingivalis Virulence and Inflammatory Response in Macrophage on Titanium

“…IL-12 is not toxic itself but prompts a neutrophil response that determined the severity of tissue damage [57,58], therefore our results may suggest that sitagliptin can control excessive levels of IL-12. Studies determined the important roles of MAPK and AKT signaling pathways in peri-implantitis [59][60][61]. Our study showed that P. gingivalis LPS significantly enhanced the phosphorylation of p38 MAPK, AKT and ERK while the treatment of sitagliptin decreased the phosphorylation, suggesting that sitagliptin may exert anti-inflammatory effects by inhibiting the MAPK and AKT signaling pathways.…”

Development of Cellular Signaling Pathways by Bioceramic Heat Treatment (Sintering) in Osteoblast Cells

“…The MAPK signaling cascade pathway, an important signaling pathway known to be involved in the regulation of osteoblast physiology, plays a major role in several processes, including cell proliferation, death, and differentiation [ 33 ]. This signaling pathway consists of several components, including JNK and p38 [ 34 ]. JNK signaling is broadly activated by oxidative stress and acts as a regulator for several life cycle processes, including cellular meiosis, mitosis, differentiation, and energy metabolism [ 35 ].…”