Silica nanoparticles enhance autophagic activity, disturb endothelial cell homeostasis and impair angiogenesis

Duan, Junchao; Yu, Yizhi; Yu, Yang; Yang, Li; Huang, Peili; Zhou, Xianqing; Peng, Shuangqing; Sun, Zhiwei

doi:10.1186/s12989-014-0050-8

Cited by 117 publications

(74 citation statements)

References 53 publications

(59 reference statements)

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“…Unlike CQ, NBP/TiO 2 nanostructures did not alter the lysosomal acidity (Figure 4b), but they did induce clear lysosome dilatation (Figure 4a). Furthermore, the intracellular cytoskeleton component F‐actin is related to the fusion between autophagosomes and lysosomes 28. Similar to BafA1, NBP/TiO 2 nanostructures disrupted the distribution of intracellular F‐actin (Figure S4, Supporting Information).…”

Section: Resultsmentioning

confidence: 87%

Titania‐Coated Gold Nano‐Bipyramids for Blocking Autophagy Flux and Sensitizing Cancer Cells to Proteasome Inhibitor‐Induced Death

et al. 2017

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Targeting protein degradation is recognized as a valid approach to cancer therapy. The ubiquitin–proteasome system (UPS) and the autophagy–lysosome pathway are two major pathways for intracellular protein degradation. Proteasome inhibitors such as bortezomib are clinically approved for treating malignancies, but to date, they are still unsatisfactory for cancer therapy. This study identifies titania‐coated gold nano‐bipyramid (NBP/TiO2) nanostructures as an autophagic flux inhibitor, as the smallest NBP/TiO2 nanostructures induce significant autophagosome accumulation in human glioblastoma U‐87 MG cells via blocking the autophagosome–lysosome fusion process and inhibiting lysosomal degradation. Further study indicates that NBP/TiO2 nanostructures reduce the intracellular level of mature cathepsin B and directly inhibit the proteolytic activity of cathepsin B, thereby further inhibiting trypsin‐like proteolytic activity, which is a potential cotarget for UPS inhibition. NBP/TiO2 nanostructures interact synergistically with bortezomib to suppress the viability of U‐87 MG cells, as the combined treatment synergistically induces the intracellular accumulation of ubiquitinated protein and endoplasmic reticulum stress. In addition, photothermal therapy further synergistically reduces the cell viability. In summary, this study suggests that NBP/TiO2 nanostructures function as a promising anticancer agent in combination with proteasome inhibitors.

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Section: Resultsmentioning

confidence: 87%

Titania‐Coated Gold Nano‐Bipyramids for Blocking Autophagy Flux and Sensitizing Cancer Cells to Proteasome Inhibitor‐Induced Death

et al. 2017

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“…To the best of our knowledge, few data are available in the literature about the underlying toxic-effect mechanisms of MSNPs on peripheral and brain vasculature 6,[9][10][11][12] or on neurons. 13 No data are available on the potential effect of MSNPs on neuronal activity.…”

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confidence: 99%

Mesoporous silica nanoparticles trigger mitophagy in endothelial cells and perturb neuronal network activity in a size- and time-dependent manner

Orlando¹,

Cazzaniga²,

Tringali³

et al. 2017

IJN

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Purpose Mesoporous silica nanoparticles (MSNPs) are excellent candidates for biomedical applications and drug delivery to different human body areas, the brain included. Although toxicity at cellular level has been investigated, we are still far from using MSNPs in the clinic, because the mechanisms involved in the cellular responses activated by MSNPs have not yet been elucidated. Materials and methods This study used an in vitro multiparametric approach to clarify relationships among size, dose, and time of exposure of MSNPs (0.05–1 mg/mL dose range), and cellular responses by analyzing the morphology, viability, and functionality of human vascular endothelial cells and neurons. Results The results showed that 24 hours of exposure of endothelial cells to 250 nm MSNPs exerted higher toxicity in terms of mitochondrial activity and membrane integrity than 30 nm MSN at the same dose. This was due to induced cell autophagy (in particular mitophagy), probably consequent to MSNP cellular uptake (>20%). Interestingly, after 24 hours of treatment with 30 nm MSNPs, very low MSNP uptake (<1%) and an increase in nitric oxide production (30%, P <0.01) were measured. This suggests that MSNPs were able to affect endothelial functionality from outside the cells. These differences could be attributed to the different protein-corona composition of the MSNPs used, as suggested by sodium dodecyl sulfate polyacrylamide-gel electrophoresis analysis of the plasma proteins covering the MSNP surface. Moreover, doses of MSNPs up to 0.25 mg/mL perturbed network activity by increasing excitability, as detected by multielectrode-array technology, without affecting neuronal cell viability. Conclusion These results suggest that MSNPs may be low-risk if prepared with a diameter <30 nm and if they reach human tissues at doses <0.25 mg/mL. These important advances could help the rational design of NPs intended for biomedical uses, demonstrating that careful toxicity evaluation is necessary before using MSNPs in patients.

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“…Their findings demonstrated that Nano SiO 2 can induce autophagic activity, accompanied by NO/NOS system disorder and an inflammatory response, eventually leading to endothelial cell dysfunction via the inhibition of the PI3K/Akt/mTOR signaling pathway. Their findings also confirm that Nano SiO 2 induced endothelial cell dysfunction is associated with autophagy, which may be an important mechanism and adverse outcome pathway of cardiovascular diseases caused by nanoparticles [33]. JunchaoDuan and his team found that the cardiovascular toxicity triggered by SiNPs occurs mainly in vascular endothelium rather than cardiomyocytes.…”

Section: Nano Siomentioning

confidence: 71%

“…Duan and his team found that SiNPs induce autophagic activity in endothelial cells and pericytes, subsequently disturb the endothelial cell homeostasis and impair angiogenesis. The VEGFR2 mediated autophagy pathway may play a critical role in maintaining endothelium and vascular homeostasis [33]. The typically morphological characteristics (autophagosomes and autolysosomes) of the autophagy process were observed in TEM ultra structural analysis by Yu's team [34].…”

mentioning

confidence: 99%

The Role of Cell Autophagy in Toxicity Caused by Dental Nanomaterials

Wei¹

2017

NTMB

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NanomaterialsThe overview of nanomaterials Nanomaterials are defined as materials composed of unbound particles or particles in an aggregate or agglomerate state with one or more external dimensions with a size ranging from 1nm to 100nm [1]. Nanomaterials have a lot of free surfaces and interfaces and there is interaction between the various units. Based on the above characteristics, nanomaterials are featured by surface effect, small size effect, quantum size effect, macroscopic quantum tunneling effect and the dielectric confinement effect. Nanoparticles have lots of unpaired atoms, large specific surface area, less surface defects and can occur in conjunction with the polymer stronger physically or chemically. Added to the polymer material, they can improve the ductility, toughness, strength, barrier properties, heat resistance and dimensional stability of the material. They have been widely used in conventional materials, medical equipment, electronic equipment, paint and other industries. However, nanomaterials will affect the organism and produce a series of toxic effects by inducing oxidative stress and inflammatory response mechanisms in the cell, subcellular and protein levels. The nanomaterials commonly used in dentistryNanometer materials are widely applied in the field of dentistry, including dental restoration, antibacterial, caries treatment, orthodontic, root canal, bonding systems and so on.Adding nanoparticles to dental restoration materials to improve the performance has been widely used in the clinical field. In view of its unpaired atoms, large specific surface area, less surface defects and occurring in conjunction with the polymer either stronger physically or chemically, the novel resin composite exhibited a strong antibacterial property upon the addition of up to 5% nano antibacterial inorganic fillers, there by leading to effective caries inhibition in dental application [2]. The mesoporous silica biomaterials have great potential for serving as both a catalyst and carrier in the repair or regeneration of dental hard tissue [3]. Diatomite-based nanocomposite ceramics are good potential candidates for ceramic-based dental materials [4]. Nano silicon dioxide can also give polymers the characteristics of better viscosity, thermal stability, high strength, less volume shrinkage and of course, durability [5].In clinical endodontics especially root canal and restorative treatments we can see the near future potential of nanoparticles from the application of nanoparticles in the form of solutions for irrigation, medication and as an additive within sealers/restorative materials [6]. GICs can be applied to base plates of Orthodontic and modified denture base well, as which contain chlorhexidine hexametaphosphate nanoparticles and characterize the nanoparticle size shows a stronger antimicrobial activity [7].As for caries treatment, Hannig M said that Analysis of in vitro data indicates that apatite nanoparticles might be effective in reversing lesion progression in the outer but not in the deepe...

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Silica nanoparticles enhance autophagic activity, disturb endothelial cell homeostasis and impair angiogenesis

Cited by 117 publications

References 53 publications

Titania‐Coated Gold Nano‐Bipyramids for Blocking Autophagy Flux and Sensitizing Cancer Cells to Proteasome Inhibitor‐Induced Death

Titania‐Coated Gold Nano‐Bipyramids for Blocking Autophagy Flux and Sensitizing Cancer Cells to Proteasome Inhibitor‐Induced Death

Mesoporous silica nanoparticles trigger mitophagy in endothelial cells and perturb neuronal network activity in a size- and time-dependent manner

The Role of Cell Autophagy in Toxicity Caused by Dental Nanomaterials

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