TNF-α was involved in calcium hydroxide-promoted osteogenic differentiation of human DPSCs through NF-κB/p38MAPK/Wnt pathway.

Abstract

It has been reported that calcium hydroxide can induce proliferation, migration, and mineralization in dental pulp stem cells (DPSCs), but the underlying molecular mechanisms are still unclear. In this study, we sought to explore the role of calcium hydroxide in the cell proliferation and directional differentiation of DPSCs and to study the regulatory effect of NF-κB, p38MAPK, and Wnt signaling on differentiation of DPSCs. CCK8 cell assay, Wound Healing Assay, and Alkaline Phosphatase Staining Assay were respectively used to determine the proliferation rate, migration and ALP expression of DPSCs. Alizarin Red Staining Assay was used to observe the mineralization of DPSCs. RT-PCR analysis and Western Blot Analysis displayed the expression of related fators at mRNA and protein level, respectively. In the present study, we found that NF-κB, p38MAPK, and Wnt signaling could abolish calcium hydroxide-induced proliferation of DPSCs. The inhibition of NF-κB, p38MAPK, and Wnt signaling suppressed the migration, ALP expression, and mineralization of DPSCs. NF-κB, p38MAPK, and Wnt signaling involved in directional differentiation of DPSCs. Moverover, calcium hydroxide could activate NF-κB, p38MAPK, and Wnt pathway by regulating TNF-α. Our study showed that NF-κB, p38MAPK, and Wnt signaling pathway were involved in calcium hydroxide-induced proliferation, migration, mineralization, and osteogenic differentiation in DPSCs. Calcium hydroxide affected NF-κB, p38MAPK, and Wnt pathway by regulating TNF-α.