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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Blotting, Western, Cell Culture Techniques, Cell Movement, Cell Survival, Coloring Agents, Dental Materials, Dental Pulp, Dose-Response Relationship, Drug, Enzyme Inhibitors, Focal Adhesion Kinase 1, Glycogen Synthase Kinase 3, Humans, Imidazoles, MAP Kinase Signaling System, Methacrylates, Mitogen-Activated Protein Kinases, Stem Cells, Tetrazolium Salts, Thiazoles, p38 Mitogen-Activated Protein Kinases.
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Does 2-Hydroxyethyl methacrylate inhibit migration of dental pulp stem cells? Context: Cell migration is an important step in pulpal wound healing. Although components in the resin-based dental materials are known to have adverse effects on pulp wound healing including proliferation and mineralization, their effects on cell migration have been scarcely examined. Here, we investigated the effects of 2-hydroxyethyl methacrylate (HEMA) on the migration of dental pulp stem cells (DPSC) in vitro. Cell viability was assessed using the MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay, and cell migration was evaluated using the wound scratch assay and transwell migration assay at noncytotoxic doses. The Western blot was used to examine pathways associated with migration such as focal adhesion kinase, mitogen-activated protein kinase, and glycogen synthase kinase 3. There were no drastic changes in the cell viability below 3 mmol/L HEMA. When DPSCs were treated with HEMA at 0.5, 1.0, and 2.5 mmol/L, cell migration was diminished. HEMA-treated DPSCs exhibited the loss of phosphorylated focal adhesion kinase in a dose-dependent manner. The HEMA-mediated inhibition of cell migration was associated with phosphorylation of p38 but not glycogen synthase kinase 3, Extracellular signal-related kinase (ERK), or c-Jun N-terminal kinase (JNK) pathways. When we inhibited the p38 signaling pathway using a p38 inhibitor, the migration of DPSCs was suppressed.
assistant
HEMA inhibits the migration of dental pulp cells in vitro, suggesting that poor pulpal wound healing under resin-based dental materials may be caused, in part, by the inhibition of cell migration by HEMA. Final Decision: yes