Suppr超能文献

力诱导一氧化氮促进小鼠正畸牙齿移动过程中的成骨活性。

Force-Induced Nitric Oxide Promotes Osteogenic Activity during Orthodontic Tooth Movement in Mice.

作者信息

Sun Yuqing, Fu Jingfei, Lin Feiran, Li Shengnan, Du Juan, Liu Yi, Bai Yuxing

机构信息

Department of Orthodontics, School of Stomatology, Capital Medical University, China.

Laboratory of Tissue Regeneration and Immunology and Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, China.

出版信息

Stem Cells Int. 2022 Sep 6;2022:4775445. doi: 10.1155/2022/4775445. eCollection 2022.

Abstract

OBJECTIVES

The aim of this study was to investigate the effect of nitric oxide (NO) on orthodontic tooth movement and the regulatory effect on bone formation.

DESIGN

A mouse orthodontic tooth movement model was established to measure the level of releasing NO. Besides, orthodontic tooth movement distance and the bone formation in the tension side of the orthodontic tooth were also analyzed. In vitro, human periodontal ligament stem cells (hPDLSCs) were cultured under tensile force stimulation. The production of NO and the expression level of nitric oxide synthase (NOS) were detected after mechanical stimulation. Furthermore, the downstream cellular signaling pathway regulated by NO was also explored.

RESULTS

The generation of NO steadily increased throughout the orthodontic tooth movement in mice. Orthodontic tooth movement was decreased in the NOS inhibitor group while it was accelerated in the NO precursor group. Force-induced NO promoted the osteogenic differentiation of human hPDLSCs under tensile force stimulation. And force-induced NO in hPDLSCs regulated the PI3K/Akt/-catenin signal pathway.

CONCLUSION

NO is involved in the regulation of orthodontic tooth movement and promotes bone formation on the tension side of the orthodontic tooth. The PI3K/Akt/-catenin pathway is one of the downstream cell signal transduction pathways of NO in the orthodontic process.

摘要

目的

本研究旨在探讨一氧化氮(NO)对正畸牙齿移动的影响以及对骨形成的调节作用。

设计

建立小鼠正畸牙齿移动模型以测量NO释放水平。此外,还分析了正畸牙齿移动距离以及正畸牙齿张力侧的骨形成情况。在体外,将人牙周膜干细胞(hPDLSCs)在拉伸力刺激下进行培养。机械刺激后检测NO的产生以及一氧化氮合酶(NOS)的表达水平。此外,还探索了由NO调节的下游细胞信号通路。

结果

在小鼠正畸牙齿移动过程中,NO的生成稳步增加。NOS抑制剂组的正畸牙齿移动减少,而NO前体组的正畸牙齿移动加速。力诱导的NO在拉伸力刺激下促进了人hPDLSCs的成骨分化。并且hPDLSCs中力诱导的NO调节了PI3K/Akt/β-连环蛋白信号通路。

结论

NO参与正畸牙齿移动的调节,并促进正畸牙齿张力侧的骨形成。PI3K/Akt/β-连环蛋白途径是正畸过程中NO的下游细胞信号转导途径之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9580/9470363/16780e98f0b6/SCI2022-4775445.001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验