The size-dependent effects of silica nanoparticles on endothelial cell apoptosis through activating the p53-caspase pathway. (February 2018)

• Record Type: Journal Article
• Authors: Wang, Wuxiang; Zeng, Can; Feng, Yuqin; Zhou, Furong; Liao, Fen; Liu, Yuanfeng; Feng, Shaolong; Wang, Xinming
• Is Part Of: Environmental pollution. Volume 233(2018)
• Page Start: 218
• Page End: 225
• Publication Date: 2018-02
• Subjects: Silica nanoparticle (SiNP) -- Endothelial cell (EC) -- Apoptosis -- p53; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2017.10.053
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: With the growing production and applications of silica nanoparticles (SiNPs), human exposure to these nanoparticles continues to increase. However, the possible hazards that SiNP exposure may pose to human cardiovascular system and the underlying mechanisms remain unclear. In the present study, the flow cytometry was employed to investigate the potential of four sizes (10, 25, 50, 100 nm) of SiNPs to induce the apoptosis of human umbilical vein endothelial cells (HUVECs) in culture. The apoptotic pathway was also explored through the determination of the protein expression and/or activation of p53, Bcl-2, Bax, caspases-9, -7, -3, and PARP by western blot. The results showed that all the four sizes of SiNPs could significantly elicit apoptosis in HUVECs at the tested concentrations (1, 5, 25 μg/mL), compared with the negative control (p < 0.05, p < 0.01). Moreover, the apoptotic rates were increased with the elevating levels and decreasing sizes of administrative SiNPs, showing both dose- and size-dependent effect relationships. Interestingly, the enhancing phosphorylation of p53 protein (Ser15), decreasing ratio of Bcl-2/Bax protein, and elevating activation of the downstream proteins, caspase-9, -7, -3 and PARP, were also observed with the decreasing sizes of tested SiNPs, indicating that the p53-caspase pathway is the main way of the SiNP-mediated apoptosis in HUVECs and that the size is an important parameter that determines the SiNPs' potential to induce cellular response. Graphical abstract: Image 1 Highlights: This study explored the apoptotic effects of SiNPs on endothelial cells and underlying molecular mechanism. The SiNPs may cause significant apoptosis to HUVECs in culture, with a clear dose- and size-dependent effect relationships. SiNP exposure may pose potential risks to human cardiovascular health via inducing EC apoptosis by the p53-caspase pathway. The size is an important parameter that determines SiNPs' potential to elicit cellular responses. Abstract : The SiNPs may cause significant apoptosis to HUVECs in culture by activating the p53-caspase pathway, and the size is an important parameter that determines their potential to elicit cellular response.