Effects of triclosan exposure on stem cells from human exfoliated deciduous teeth (SHED) fate

被引:5
作者
Deng, Shiwen [1 ]
Li, Caifeng [1 ]
Chen, Junqi [2 ]
Cui, Zhao [3 ]
Lei, Tong [1 ]
Yang, Hongjun [1 ]
Chen, Peng [1 ,4 ]
机构
[1] China Acad Chinese Med Sci, Expt Res Ctr, Beijing Key Lab Tradit Chinese Med Basic Res Preve, Beijing 100700, Peoples R China
[2] Shandong First Med Univ & Shandong Acad Med Sci, Sch Pharm & Pharmaceut Sci, Jinan 250117, Shandong, Peoples R China
[3] China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China
[4] Hunan Prov Key Lab Complex Effects Anal Chinese Pa, Yongzhou 425199, Hunan, Peoples R China
关键词
Triclosan; SHED; Toxicity response; Transcriptome; PTEN/PI3K/AKT/mTOR axis; SIGNALING PATHWAY; CYCLE ARREST; INHIBITION; APOPTOSIS; AUTOPHAGY; TOXICITY; TISSUE;
D O I
10.1016/j.scitotenv.2023.167053
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Triclosan (TCS), a widely used broad-spectrum antibacterial agent and preservative, is commonly found in products and environments. Widespread human exposure to TCS has drawn increasing attention from researchers concerning its toxicological effect. However, minimal studies have focused on the impact of TCS exposure on human stem cells. Therefore, the aim of the present study was to evaluate the effects of TCS exposure on stem cells from human exfoliated deciduous teeth (SHED) and its molecular mechanisms. A series of exper-imental methods were conducted to assess cell viability, morphology, proliferation, differentiation, senescence, apoptosis, mitochondrial function, and oxidative stress after SHED exposure to TCS. Furthermore, transcriptome analysis was applied to investigate the response of SHED to different concentrations of TCS exposure and to explore the molecular mechanisms. We demonstrated that TCS has a dose-dependent proliferation and differentiation inhibition of SHED, while promoting cellular senescence, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and oxidative stress, as well as significantly induces apoptosis and autophagy flux inhibition at high concentrations. Interestingly, no significant morphological changes in SHED were observed after TCS exposure. Transcriptome analysis of normal and TCS-induced SHED suggested that SHED may use different strategies to counteract stress from different concentrations of TCS and showed significant differences. We discovered that TCS mediates cellular injury of SHED by enhancing the expression of PTEN, thereby inhibiting the phosphorylation levels of PI3K and AKT as well as mTOR expression. Collectively, our findings provide a new understanding of the toxic effects of TCS on human stem cell fate, which is important for determining the risk posed by TCS to human health.
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页数:18
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