4.6 Article

Concentration-Dependent Cellular Uptake of Graphene Oxide Quantum Dots Promotes the Odontoblastic Differentiation of Dental Pulp Cells via the AMPK/mTOR Pathway

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ACS OMEGA
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AMER CHEMICAL SOC
DOI: 10.1021/acsomega.2c06508

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As zero-dimension nanoparticles, graphene oxide quantum dots (GOQDs) have the potential to regulate cell proliferation and differentiation. This study investigated the effect and molecular mechanism of GOQDs on the odontoblastic differentiation of dental pulp cells (DPSCs). The results showed that low concentrations of GOQDs promoted the proliferation and odontoblastic differentiation of DPSCs, possibly through the activation of the AMPK signaling pathway and inhibition of the mTOR signaling pathway.
As zero-dimension nanoparticles, graphene oxide quantum dots (GOQDs) have broad potential for regulating cell proliferation and differentiation. However, such regulation of dental pulp cells (DPSCs) with different concentrations of GOQDs is insufficiently investigated, especially on the molecular mechanism. The purpose of this study was to explore the effect and molecular mechanism of GOQDs on the odontoblastic differentiation of DPSCs and to provide a theoretical basis for the repair of pulp vitality by pulp capping. CCK-8, immunofluorescence staining, alkaline phosphatase activity assay and staining, alizarin red staining, qRT-PCR, and western blotting were used to detect the proliferation and odontoblastic differentiation of DPSC coculturing with different concentrations of GOQDs. The results indicate that the cellular uptake of low concentration of GOQDs (0.1, 1, and 10 mu g/mL) could promote the proliferation and odontoblastic differentiation of DPCSs. Compared with other concentration groups, 1 mu g/mL GOQDs show better ability in such promotion. In addition, with the activation of the AMPK signaling pathway, the mTOR signaling pathway was inhibited in DPSCs after coculturing with GOQDs, which indicates that low concentrations of GOQDs could regulate the odontoblastic differentiation of DPSCs by the AMPK/mTOR signaling pathway.

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