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应激对乳牙牙周膜干细胞生物学特性及代谢的影响

Effects of Stress on Biological Characteristics and Metabolism of Periodontal Ligament Stem Cells of Deciduous Teeth.

作者信息

Li Zhengyang, Li Jinyi, Dai Shanshan, Su Xuelong, Ren Meiyue, He Shuyang, Guo Qingyu, Liu Fei

机构信息

Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China; Department of Pediatric Dentistry, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.

Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-Sen University, Guangzhou, Guangdong, China; Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, Guangdong, China.

出版信息

Int Dent J. 2025 Apr;75(2):908-920. doi: 10.1016/j.identj.2024.09.011. Epub 2024 Oct 5.

DOI:10.1016/j.identj.2024.09.011
PMID:39370340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11976548/
Abstract

INTRODUCTION AND AIMS

Periodontal ligament stem cells (PDLSCs) from deciduous teeth (DePDLSCs) can perceive and respond to mechanical signals upon exposure to various environments. The effects of mechanical stress on the biological characteristics and metabolism of DePDLSCs were investigated using in vitro stress loading.

METHODS

DePDLSCs were subjected to mechanical stresses of different strengths. Cell proliferation, expression of osteogenic/osteoclastic factors, apoptosis, and oxidative stress levels were evaluated using CCK-8 assays, alkaline phosphatase staining, real-time PCR, flow cytometry, and malondialdehyde and superoxide dismutase assays. Liquid chromatography-mass spectrometry was used to perform nontargeted metabolomic detection and analysis.

RESULTS

Under stresses of 75 and 150 kPa, the expression of osteogenesis-related factors OPG, ALP, and RUNX2 decreased, and the ratio of RANKL/OPG significantly increased. A pressure of 150 kPa induced oxidative stress and caused a significant increase in cell apoptosis. Among the differential metabolites screened from the 150 kPa group, spermine, spermidine, ceramide, phosphatidylethanolamine, lysophosphatidylethanolamine, linoleic acid, and docosatrienoic acid were the most significantly upregulated. The metabolites screened from the 75 kPa group were mainly related to glycerophospholipid and sphingolipid metabolism, oxidative phosphorylation, and mineral absorption, which were common pathways affected in both experimental groups.

CONCLUSION

A certain degree of mechanical stress can inhibit the proliferative activity and osteogenic differentiation of DePDLSCs, enhance their osteoclast-inducing ability, and cause elevated levels of cell apoptosis and oxidative stress. The metabolic expression profile of DePDLSCs changed significantly under stress. Understanding changes in cellular activity and metabolic reactions may provide an experimental basis for elucidating the role of mechanical stress in root resorption and periodontal tissue remodelling of deciduous teeth.

CLINICAL RELEVANCE

Mechanical stress may affect periodontal tissue remodeling and root resorption of DePDLSc.

摘要

引言与目的

来自乳牙的牙周膜干细胞(DePDLSCs)在暴露于各种环境时能够感知并响应机械信号。本研究通过体外应力加载,探究机械应力对DePDLSCs生物学特性和代谢的影响。

方法

对DePDLSCs施加不同强度的机械应力。使用CCK-8法、碱性磷酸酶染色、实时定量PCR、流式细胞术以及丙二醛和超氧化物歧化酶检测法,评估细胞增殖、成骨/破骨因子表达、细胞凋亡和氧化应激水平。采用液相色谱-质谱联用技术进行非靶向代谢组学检测与分析。

结果

在75 kPa和150 kPa应力作用下,成骨相关因子OPG、ALP和RUNX2的表达降低,RANKL/OPG比值显著升高。150 kPa的压力诱导氧化应激并导致细胞凋亡显著增加。在150 kPa组筛选出的差异代谢物中,精胺、亚精胺、神经酰胺、磷脂酰乙醇胺、溶血磷脂酰乙醇胺、亚油酸和二十二碳三烯酸上调最为显著。75 kPa组筛选出的代谢物主要与甘油磷脂和鞘脂代谢、氧化磷酸化以及矿物质吸收有关,这些是两个实验组中均受影响的常见途径。

结论

一定程度的机械应力可抑制DePDLSCs的增殖活性和成骨分化,增强其诱导破骨细胞的能力,并导致细胞凋亡和氧化应激水平升高。应激状态下DePDLSCs的代谢表达谱发生显著变化。了解细胞活性和代谢反应的变化,可为阐明机械应力在乳牙牙根吸收和牙周组织重塑中的作用提供实验依据。

临床意义

机械应力可能影响DePDLSc的牙周组织重塑和牙根吸收。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/efb02a4908e6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/6538d0417a4a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/6d62ec3af321/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/d4346367597f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/7d57716f2bc6/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/4325dc70e9b6/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/efb02a4908e6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/6538d0417a4a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/6d62ec3af321/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/d4346367597f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/7d57716f2bc6/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/4325dc70e9b6/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/848d/11976548/efb02a4908e6/gr6.jpg

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