Key Role of TFEB Nucleus Translocation for Silver Nanoparticle‐Induced Cytoprotective Autophagy

Lin, Jun; Liu, Yiming; Wu, Hao; Huang, Zhihai; Ma, Jingfan; Guo, Chang; Gao, Feng; Jin, Peipei; Wei, Pengfei; Zhang, Yunjiao; Liu, Liu; Zhang, Rui; Qiu, Longxin; Gu, Ning; Wen, Longping

doi:10.1002/smll.201703711

Cited by 40 publications

(37 citation statements)

References 40 publications

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“…Although other NMs have been reported to target lysosomes, the detailed molecular mechanisms are still unclear. We speculated that ZNPs activated lysosomal biogenesis, which is supported by other studies . They indicated that NMs activated lysosome biogenesis due to the nucleus translocation of transcription factor EB (TFEB), which regulates the expression of genes encoding lysosomal proteins and the processing of lysosomal proteins.…”

Section: Discussionsupporting

confidence: 62%

“…Nanotechnology is being a new approach to detect and intervene in certain biological processes that involve vesicular compartments, such as endosomes, lysosomes, and autophagosomes, as the major sites of nanoparticles (NPs) accumulation in cells. Several nanomaterials (NMs), such as gold, silver, and carbon‐based nanomaterials, induce autophagy as their main biological effect. Therein, autophagy is activated to eliminate foreign materials, which is important for cellular self‐protection, and recycling of the damaged proteins and organelles is promoted as well to sustain the metabolism homeostasis .…”

Section: Introductionmentioning

confidence: 99%

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Key Role of Microtubule and Its Acetylation in a Zinc Oxide Nanoparticle–Mediated Lysosome–Autophagy System

Liu

Kang

Yin

et al. 2019

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Autophagy is a biological process that has attracted considerable attention as a target for novel therapeutics. Recently, nanomaterials (NMs) have been reported to modulate autophagy, which makes them potential agents for the treatment of autophagy‐related diseases. In this study, zinc oxide nanoparticles (ZNPs) are utilized to evaluate NM‐induced autophagy and debate the mechanisms involved. It is found that ZNPs undergo pH‐dependent ion shedding and that intracellular zinc ions (Zn2+) play a crucial role in autophagy. Autophagy is activated with ZNPs treatment, which is inhibited after Zn2+ sequestration via ethylenediamine tetra‐acetic acid. Lysosome‐based autophagic degradation is halted after ZNPs treatment for more than 3 h and is accompanied by blockage of lysophagy, which renews impaired lysosomes. Furthermore, the microtubule (MT) system participates in ZNP‐induced lysosome–autophagy system changes, especially in the fusion between autophagosomes and lysosomes. MT acetylation is helpful for protecting from ZNP‐induced MT disruption, and it promotes the autophagic degradation process. In conclusion, this study provides valuable information on NM‐induced lysosome–autophagy system changes, particularly with respect to the role of lysophagy and the MT system, which point to some attractive targets for the design of engineered nanoparticles.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Key Role of Microtubule and Its Acetylation in a Zinc Oxide Nanoparticle–Mediated Lysosome–Autophagy System

Liu

Kang

Yin

et al. 2019

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“…Both mTORC1 and ERK1/2 are negative regulators of TFEB and make the TFEB dephosphorylation, leading to TFEB translocates into the nucleus to execute its function, and thereby promoting autophagy and lysosome biogenesis‐related genes expression. A recent report has shown that the AgNP‐induced autophagy is mediated by TFEB, while the AgNP‐induced TFEB nucleus translation is independent of mTOR1 and ERK1/2 . In the AgNP‐treated cells, the AgNP‐induced TFEB nucleus translocation leads to the elevated level of autophagy serving as a protective mechanism in cell.…”

Section: Nm‐phagy‐related Moleculesmentioning

confidence: 98%

“…The transcription factor EB (TFEB) regulates NM‐phagy by upregulating autophagy‐related genes, and similar to LC3B, UVRAG, and p62, it can control lysosomal biogenesis . In the CeO 2 NP‐treated cells, the CeO 2 NPs help TFEB translocate from cytoplasm into nucleus and promote autophagy induction .…”

Section: Nm‐phagy‐related Moleculesmentioning

confidence: 99%

Crosstalk between Autophagy and Nanomaterials: Internalization, Activation, Termination

Wei

Duan

2018

Adv. Biosys.

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NMs, SiO 2 -based NMs, lipid-based NMs, polymer-based NMs, polyethylene glycol (PEG)-based NMs, and other types NMs. Alternatively, according to the physical and chemical properties of NMs, they can be classified into soft NMs, referring to lipidor polymer-based NMs, and hard NMs such as mental-or carbon-based NMs.With the development of nanotechnology, these materials have been widely applied in various fields. [3] For example, ZnO nanoparticles (NPs) can serve as antimicrobial agents; [4] TiO 2 NPs are used in sunscreen lotions; [5] lipid/polymeric-based NPs are applied in drug/gene delivery; [6] QDs are used as florescent probes; [7] and magnetic NPs are applied in magnetic resonance imaging. [8] The NMs not only effectively enhance cellular and subcellular targeting of drugs and the effect of imaging, but also rise the attention on the importance of affirming the effect of NMs on biological systems. It has been recognized that NMs are capable of modulating autophagy. The modulation of NMs on autophagy may be beneficial, since the combinative effect of the NMs' features and autophagy functions is capable of enhancing the accuracy of diagnosis and efficiency of therapies. For example, AgNPs could be a fascinating tool in infections and antimicrobial immunity in that the NM-phagy can modulate the antiviral/antibacterial defenses. [9] In this process, AgNPs lead to the disorganization of mitochondrial network and contribute to the modulation of autophagy (both Rab9-dependent alternative autophagy and Atg-5-dependent classical autophagy) by blocking the autophagic flux. Additionally, AgNPs can reduce the production of CCL-5 and interferon (IFN)-β in influenza-infected cells through the Rab9-dependent alternative autophagy.Autophagy, a "self-digestion" biological process of cellular degradation, is induced when cells are subjected to unfavorable factors, including starvation or drug treatments, accumulation of the damaged organelles, and misfolded proteins. The autophagic process refers to the cargo encompassed into autophagosome and delivery of cargo to lysosomes to degrade and to release macromolecules back into the cytosol. [10] If the "self-digestion" gets out of control, the autophagy dysfunction, including excessive autophagy induction or suppression of autophagy flux, will induce serious diseases, such as cancer, neurodegenerative diseases, immunological diseases, innate turbulence, and even cell death. [11] Therefore, autophagy is Nanomaterials (NMs) are comprehensively applied in biomedicine due to their unique physical and chemical properties. Autophagy, as an evolutionarily conserved cellular quality control process, is closely associated with the effect of NMs on cells. In this review, the recent advances in NM-induced/ inhibited autophagy (NM-phagy) are summarized, with an aim to present a comprehensive description of the mechanisms of NM-phagy from the perspective of internalization, activation, and termination, thereby bridging autophagy and nanomaterials. Several possible mechanisms are extensively ...

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“…PVP is one of the common nanosilver coatings used in experiments to stabilize the nanosilver and prevent aggregation [42]. The effects of PVP itself has been tested at the appropriate experimental concentrations on cells and found to not cause the effects that are observed when the cells are treated with PVP-coated nanosilver [42][43][44]. Citrate is another common stabilizer, and on its own did not decrease the life span of Drosophila melanogaster [18].…”

Section: Introductionmentioning

confidence: 99%

A Current Overview of the Molecular Effects of Nanosilver

Cameron¹,

Willmore²

2018

Preprint

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Nanosilver plays an important role in nanoscience and nanotechnology, and is becoming increasingly used for applications in nanomedicine. Nanosilver ranges in size from one to one hundred nanometers. Smaller particles more readily enter cells and interact with the cellular components. The exposure dose, particle size, coating, and aggregation state of the nanosilver, as well as the cell type or organism that it is tested on, all have a large determining factor on the effect and potential toxicity of nanosilver. A high exposure dose to nanosilver alters the cellular stress responses and initiates cascades of signaling that can eventually trigger organelle autophagy and apoptosis. This review summarizes the current knowledge of the effects of nanosilver on cellular metabolic function and response to stress. Both the causative effects of nanosilver on oxidative stress, endoplasmic reticulum stress, and hypoxic stress, as well as the effects of nanosilver on the responses to such stresses, are outlined. The interactions and effects of nanosilver on cellular uptake, oxidative stress (reactive oxygen species), inflammation, hypoxic response, mitochondrial function, endoplasmic reticulum function and the unfolded protein response, autophagy and apoptosis, angiogenesis, epigenetics, genotoxicity, and cancer development and tumorigenesis, as well as other pathway alterations are examined in this review.

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Key Role of TFEB Nucleus Translocation for Silver Nanoparticle‐Induced Cytoprotective Autophagy

Cited by 40 publications

References 40 publications

Key Role of Microtubule and Its Acetylation in a Zinc Oxide Nanoparticle–Mediated Lysosome–Autophagy System

Key Role of Microtubule and Its Acetylation in a Zinc Oxide Nanoparticle–Mediated Lysosome–Autophagy System

Crosstalk between Autophagy and Nanomaterials: Internalization, Activation, Termination

A Current Overview of the Molecular Effects of Nanosilver

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