CTHRC1对人牙髓干细胞成牙分化和血管生成的影响。

Jong-Soon Kim, Bin-Na Lee, Hoon-Sang Chang, In-Nam Hwang, Won-Mann Oh, Yun-Chan Hwang
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引用次数: 0

摘要

目的:本研究旨在确定参与血管重塑和骨形成的胶原三螺旋重复序列-1 (CTHRC1)在人牙髓干细胞(hDPSCs)中是否能刺激成牙分化和血管生成。材料和方法:采用WST-1法评估暴露于CTHRC1的hDPSCs的生存能力。给药剂量分别为5、10和20µg/mL的CTHRC1给药于hdpsc。采用逆转录聚合酶法检测牙本质唾液磷蛋白、牙本质基质蛋白1、血管内皮生长因子和成纤维细胞生长因子2。用茜素红评价了矿化结核的形成。通过抓伤实验来评估CTHRC1对细胞迁移的影响。数据分析采用单因素方差分析,随后采用Tukey事后检验。差异有统计学意义的阈值为p < 0.05。结果:5、10、20µg/mL的CTHRC1剂量对hdpsc的活力无显著影响。矿化结节形成,牙源性标志物上调,表明CTHRC1促进了牙源性分化。抓伤实验表明,CTHRC1显著增强了hdpsc的迁移。结论:CTHRC1促进了hdpsc的牙源性分化和矿化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effects of CTHRC1 on odontogenic differentiation and angiogenesis in human dental pulp stem cells.

Effects of CTHRC1 on odontogenic differentiation and angiogenesis in human dental pulp stem cells.

Effects of CTHRC1 on odontogenic differentiation and angiogenesis in human dental pulp stem cells.

Effects of CTHRC1 on odontogenic differentiation and angiogenesis in human dental pulp stem cells.

Objectives: This study aimed to determine whether collagen triple helix repeat containing-1 (CTHRC1), which is involved in vascular remodeling and bone formation, can stimulate odontogenic differentiation and angiogenesis when administered to human dental pulp stem cells (hDPSCs).

Materials and methods: The viability of hDPSCs upon exposure to CTHRC1 was assessed with the WST-1 assay. CTHRC1 doses of 5, 10, and 20 µg/mL were administered to hDPSCs. Reverse-transcription polymerase reaction was used to detect dentin sialophosphoprotein, dentin matrix protein 1, vascular endothelial growth factor, and fibroblast growth factor 2. The formation of mineralization nodules was evaluated using Alizarin red. A scratch wound assay was conducted to evaluate the effect of CTHRC1 on cell migration. Data were analyzed using 1-way analysis of variance followed by the Tukey post hoc test. The threshold for statistical significance was set at p < 0.05.

Results: CTHRC1 doses of 5, 10, and 20 µg/mL had no significant effect on the viability of hDPSCs. Mineralized nodules were formed and odontogenic markers were upregulated, indicating that CTHRC1 promoted odontogenic differentiation. Scratch wound assays demonstrated that CTHRC1 significantly enhanced the migration of hDPSCs.

Conclusions: CTHRC1 promoted odontogenic differentiation and mineralization in hDPSCs.

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