Seoul National University · 歯学
Professor Hyeong-Cheol Yang's research lab focuses on the molecular mechanisms of cellular toxicity, particularly in the context of dental materials and metal ions, with an emphasis on oxidative stress, mitochondrial dysfunction, and cellular responses in mammalian and yeast models. The lab investigates how resin monomers and metal ions from dental alloys induce cytotoxicity through reactive oxygen species (ROS) generation and mitochondrial damage, while also exploring strategies to mitigate these effects. Additionally, the lab examines the role of cytoskeletal dynamics and organelle function in cell polarity and stress responses, using live-cell imaging and molecular assays. Their work bridges dental biomaterials science with cell biology and toxicology, aiming to improve the safety and biocompatibility of restorative materials.
Figures are computed from collected data and may differ slightly.
Actin cables, bundles of actin filaments that align along the long axis of budding yeast, are crucial for establishment of cell polarity. We fused green fluorescent protein (GFP) to actin binding protein 140 (Abp140p) and visualized actin cable dynamics in living yeast. We detected two populations of actin cables: (i) bud-associated cables, which extend from the bud along the mother-bud axis, and (ii) randomly oriented cables, which are relatively short. Time-lapse imaging of Abp140p-GFP reveale
Metal ions are released from dental alloys into the oral environment, which can cause biological responses over short and extended periods. Since most toxic metal ions are capable of inducing oxidative stress on cells through the mitochondrial respiratory chain, mitochondria may contribute to and be a target of metal toxicity. In this study, we investigated the effect of metal ions on growth of the budding yeast, Saccharomyces cerevisiae, and on the morphology and function of yeast mitochondria.
Dentin formation is preferred in the healing response of the pulp to pulp-capping agents during vital pulp therapy. Enhancement of the dentinogenic differentiation of dental pulp cells is thought to accelerate pulp repair. The aim of this study was to evaluate the dentinogenic activity of small molecules (three flavonoids and phenamil) that have been shown previously to induce osteoblast differentiation. Among the flavonoids (quercetin, genistein and baicalin), quercetin induced the highest alka
Inhibiting liposome uptake by macrophages using polyethylene glycol (PEG) surface modifications is a widely used approach for extending the half-life of liposomes circulating in the blood. However, the biological effects of PEGylated liposomes on macrophages have not yet been thoroughly investigated. The purpose of this study was to examine the effects of PEGylated phosphatidylserine-containing liposomes (PEG-PSLs) on the expression of two inflammation-associated cytokines, tumor necrosis factor
Triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) are major resinous components of dental restorative materials and dentin bonding adhesives. Resin monomers are known to cause cytotoxicity in mammalian cells via oxidative stress and inhibit differentiation of dental pulp cells and osteoblasts. This study was aimed to investigate whether oxidative stress was involved in the inhibition of TEGDMA- and HEMA-induced differentiation. TEGDMA and HEMA reduced alkaline phos
Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (·OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts,
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