Journal of orthodontic science · 2026
Endothelin-1 upregulates cyclooxygenase-2 expression and prostaglandin E2 synthesis in human periodontal ligament cells-an in vitro study.
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Unmanatakoon Supachai, Suttamanatwong Supaporn
Аннотация
AIMS: Endothelin-1 (ET-1) increased bone resorption during orthodontic tooth movement (OTM) in animal models, suggesting potential clinical applications for accelerating OTM. However, the molecular mechanisms by which ET-1 regulates the expression of genes involved in OTM in human periodontal ligament (hPDL) cells remain unexplored. This study investigated the effect of ET-1 on vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2) expression and PGE2 production in hPDL cells.
MATERIALS AND METHODS: hPDL cells were treated with 1, 10, and 100 pM ET-1 for 24 h, and cytotoxicity was assessed by MTT assay. The time-course and dose-response effects of ET-1 on VEGF expression were evaluated. For COX-2 expression, cells were treated with 10 pM ET-1 for 0.5, 1, 2, and 4 h. Quantitative polymerase chain reaction was used to measure VEGF and COX-2 mRNA levels, and enzyme-linked immunosorbent assay was performed to assess PGE2 production. To explore the role of the extracellular signal-regulated kinase (ERK) pathway, cells were pretreated with PD98059 before ET-1 exposure. Statistical significance was determined by one-way analysis of variance or Kruskal-Wallis test.
RESULTS: ET-1 at 1-100 pM showed no cytotoxic effects. ET-1 did not significantly affect VEGF expression at any time point or dose tested. In contrast, ET-1 significantly increased COX-2 expression and PGE2 production at 1 h (P < 0.05). PD98059 did not inhibit ET-1-induced COX-2 expression, suggesting that ET-1 regulates COX-2 via an ERK-independent mechanism.
CONCLUSION: ET-1 upregulates COX-2 expression and PGE2 synthesis in hPDL cells through an ERK-independent pathway, while exerting no significant effect on VEGF expression. Further studies are warranted to assess the therapeutic potential of ET-1 in accelerating OTM.
MATERIALS AND METHODS: hPDL cells were treated with 1, 10, and 100 pM ET-1 for 24 h, and cytotoxicity was assessed by MTT assay. The time-course and dose-response effects of ET-1 on VEGF expression were evaluated. For COX-2 expression, cells were treated with 10 pM ET-1 for 0.5, 1, 2, and 4 h. Quantitative polymerase chain reaction was used to measure VEGF and COX-2 mRNA levels, and enzyme-linked immunosorbent assay was performed to assess PGE2 production. To explore the role of the extracellular signal-regulated kinase (ERK) pathway, cells were pretreated with PD98059 before ET-1 exposure. Statistical significance was determined by one-way analysis of variance or Kruskal-Wallis test.
RESULTS: ET-1 at 1-100 pM showed no cytotoxic effects. ET-1 did not significantly affect VEGF expression at any time point or dose tested. In contrast, ET-1 significantly increased COX-2 expression and PGE2 production at 1 h (P < 0.05). PD98059 did not inhibit ET-1-induced COX-2 expression, suggesting that ET-1 regulates COX-2 via an ERK-independent mechanism.
CONCLUSION: ET-1 upregulates COX-2 expression and PGE2 synthesis in hPDL cells through an ERK-independent pathway, while exerting no significant effect on VEGF expression. Further studies are warranted to assess the therapeutic potential of ET-1 in accelerating OTM.