Endothelial cell injury and dysfunction induced by silver nanoparticles through oxidative stress via IKK/NF-κB pathways

Shi, Junpeng; Sun, Xia; Lin, Yi Hui; Zou, Xiaoyan; Liu, Zhanjun; Liao, Yulin; Du, Miaomiao; Zhang, Hongwu

doi:10.1016/j.biomaterials.2014.04.093

Cited by 138 publications

(103 citation statements)

References 34 publications

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“…10 It is a source of GSH and sulfhydryl groups, and its antioxidant activity results from its abilities to scavenge free radicals by interacting with ROS and raise levels of cellular GSH. To be noted, some reports showed an effective decline in cellular uptake of NPs in the presence of NAC, 24,25 whereas our results demonstrated that NAC pretreatment had no effect on SiNPs uptake, which might be associated with the characterization and concentration of NPs used in experiments according to the study by Davda and Labhasetwar. 26 Long et al demonstrated that ROS generation is an initial cellular response to NP internalization.…”

Section: Discussioncontrasting

confidence: 42%

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Guo¹,

Yang²,

Li³

et al. 2016

IJN

195

111

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Environmental exposure to silica nanoparticles (SiNPs) is inevitable due to their widespread application in industrial, commercial, and biomedical fields. In recent years, most investigators focus on the evaluation of cardiovascular effects of SiNPs in vivo and in vitro. Endothelial injury and dysfunction is now hypothesized to be a dominant mechanism in the development of cardiovascular diseases. This study aimed to explore interaction of SiNPs with endothelial cells, and extensively investigate the exact effects of reactive oxygen species (ROS) on the signaling molecules and cytotoxicity involved in SiNPs-induced endothelial injury. Significant induction of cytotoxicity as well as oxidative stress, apoptosis, and autophagy was observed in human umbilical vein endothelial cells following the SiNPs exposure ( P <0.05). The oxidative stress was induced by ROS generation, leading to redox imbalance and lipid peroxidation. SiNPs induced mitochondrial dysfunction, characterized by membrane potential collapse, and elevated Bax and declined bcl-2 expression, ultimately leading to apoptosis, and also increased number of autophagosomes and autophagy marker proteins, such as LC3 and p62. Phosphorylated ERK, PI3K, Akt, and mTOR were significantly decreased, but phosphorylated JNK and p38 MAPK were increased in SiNPs-exposed endothelial cells. In contrast, all of these stimulation phenomena were effectively inhibited by N -acetylcysteine. The N -acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling. In summary, the results demonstrated that SiNPs triggered autophagy and apoptosis via ROS-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling in endothelial cells, and subsequently disturbed the endothelial homeostasis and impaired endothelium. Our findings may provide experimental evidence and explanation for cardiovascular diseases triggered by SiNPs. Furthermore, results hint that the application of antioxidant may provide a novel way for safer use of nanomaterials.

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Section: Discussioncontrasting

confidence: 42%

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Guo¹,

Yang²,

Li³

et al. 2016

IJN

195

111

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“…The internalization of VE-cadherin increases endothelial monolayer permeability, which is a risk factor of early atherosclerosis [24]. In a previous study, we found that high concentrations of AgNPs could induce endothelial cell injury and dysfunction via oxidative stress and may be a potential risk factor for early atherosclerosis [25]. However, the AgNPs concentrations were not relevant to real-life exposures and were much higher than environmental concentrations.…”

Section: Introductionmentioning

confidence: 96%

Silver nanoparticles interact with the cell membrane and increase endothelial permeability by promoting VE-cadherin internalization

Sun

Shi

Zou

et al. 2016

Journal of Hazardous Materials

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“…22 In vitro studies showed that AgNPs can damage the mitochondria, and increase reactive oxygen species production and apoptosis in a p53-dependent process involving reactive oxygen species and the c-Jun N-terminal kinase cascade, or via the IKK/NF-κB pathway. [23][24][25] Thus, although the unique properties of AgNPs have led to their use in a broad range of applications, more attention has been paid to the production of AgNPs rather than to their applications. 26 Indeed, various methods for the synthesis of AgNPs have been reported in the literature.…”

Section: Introductionmentioning

confidence: 99%

Effects of silver nanoparticles on neonatal testis development in mice

Zhang¹,

Gurunathan²,

Kim³

2015

IJN

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Background Metal nanoparticles (MNPs) play an important role in consumer products. An increasing use of MNPs has raised concerns about potential risks for human health. Therefore, in vivo tests of MNPs are urgently required. Using mice as a model animal, the aim of the present study was designed to investigate the effect of biologically synthesized silver nanoparticles (AgNPs) on spermatogenesis in neonatal mice. Methods AgNPs were synthesized using Bacillus funiculus . The prepared nanoparticles were characterized using various analytical techniques such as UV–visible spectroscopy, X-ray diffraction, Fourier transform-infrared spectroscopy, and transmission electron microscopy. The prepared AgNPs were used to investigate testis development in neonatal mice. Institute of Cancer Research neonatal male mice were used in all experiments and were treated with different doses (0, 1, and 5 mg/kg) of AgNPs five times (interval of 3 days from postnatal day [PND] 8–21) by abdominal subcutaneous injection. Results The results showed that the sperm abnormalities such as quality and quantity were significantly increased by the synthesized AgNPs. The diameter of the convoluted tubules shrank significantly in mice treated with AgNPs on PND28 and PND42. The results of reverse transcription-quantitative polymerase chain reaction indicated that the E1f1ay , Gsta4 , and Fdx1 genes were up-regulated, and the Amh , Cx43 , and Claudin-11 genes were down-regulated in response to AgNPs exposure on PND28; however, these genes recovered at PND60. AgNPs had no effect on the recombination levels of chromosomes in germ cells. Conclusion These results demonstrated the adverse effects of AgNPs on the male reproductive tract, particularly spermatogenesis and the quality of sperm. This study suggests that the development of nanomaterials should be safer and non-toxic to the living organisms and the potential reprotoxicity of AgNPs should be investigated more carefully.

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Endothelial cell injury and dysfunction induced by silver nanoparticles through oxidative stress via IKK/NF-κB pathways

Cited by 138 publications

References 34 publications

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Silver nanoparticles interact with the cell membrane and increase endothelial permeability by promoting VE-cadherin internalization

Effects of silver nanoparticles on neonatal testis development in mice

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