In vitro cytotoxicity of gold nanorods in A549 cells

Tang, Ying; Shen, Yan; Huang, Libin; Lv, Gaojian; Lei, Changhai; Fan, Xiaoyan; Lin, Fangxing; Zhang, Yuxia; Wei, Lihui; Yang, Yue

doi:10.1016/j.etap.2015.02.003

Cited by 52 publications

(35 citation statements)

References 31 publications

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“…The findings of the present study, combined with previously reported studies20,21 and with more recent studies by other groups,30,31 provide indirect evidence that iron-driven ROS, generated inside lysosomes, are involved in lysosomal damage. Without access to a suitable sensor for the detection of lysosomal ROS, the importance of ROS generation has been based so far on the detection of reduced levels of ROS, and lysosomal damage, in the presence of iron chelators that specifically target the lysosomal compartment 20,21,30–32.…”

Section: Discussionsupporting

confidence: 89%

Oxidant-induced autophagy and ferritin degradation contribute to epithelial–mesenchymal transition through lysosomal iron

Sioutas¹,

Vainikka²,

Kentson³

et al. 2017

JIR

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PurposeTransforming growth factor (TGF)-β1 triggers epithelial–mesenchymal transition (EMT) through autophagy, which is partly driven by reactive oxygen species (ROS). The aim of this study was to determine whether leaking lysosomes and enhanced degradation of H-ferritin could be involved in EMT and whether it could be possible to prevent EMT by iron chelation targeting of the lysosome.Materials and methodsEMT, H-ferritin, and autophagy were evaluated in TGF-β1-stimulated A549 human lung epithelial cells cultured in vitro using Western blotting, with the additional morphological assessment of EMT. By using immunofluorescence and flow cytometry, lysosomes and ROS were assessed by acridine orange and 6-carboxy-2′,7′-dichlorodihydrofluorescein acetate assays, respectively.ResultsTGF-β1-stimulated cells demonstrated a loss of H-ferritin, which was prevented by the antioxidant N-acetyl-L-cysteine (NAC) and inhibitors of lysosomal degradation. TGF-β1 stimulation generated ROS and autophagosome formation and led to EMT, which was further promoted by the additional ROS-generating cytokine, tumor necrosis factor-α. Lysosomes of TGF-β1-stimulated cells were sensitized to oxidants but also completely protected by lysosomal loading with dextran-bound deferoxamine (DFO). Autophagy and EMT were prevented by NAC, DFO, and inhibitors of autophagy and lysosomal degradation.ConclusionThe findings of this study support the role of enhanced autophagic degradation of H-ferritin as a mechanism for increasing the vulnerability of lysosomes to iron-driven oxidant injury that triggers further autophagy during EMT. This study proposes that lysosomal leakage is a novel pathway of TGF-β1-induced EMT that may be prevented by iron-chelating drugs that target the lysosome.

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Section: Discussionsupporting

confidence: 89%

Oxidant-induced autophagy and ferritin degradation contribute to epithelial–mesenchymal transition through lysosomal iron

Sioutas¹,

Vainikka²,

Kentson³

et al. 2017

JIR

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“…Oxidative stress is one of the most common cellular outcomes associated with PM 0.1 toxicity. Increased ROS due to exposure to PM 0.1 have been shown in various cell types, including those of the respiratory system such as normal bronchial epithelial cells (NHBE) [22], Beas-2B [23,24,25], A549 [22] and human lung fibroblasts [26,27]; those with relevance to cardiovascular disease include human umbilical vein and human aorta endothelial cells (HUVEC/HAEC) [28,29] and macrophages [30]. Exposure of mouse pulmonary microvascular endothelial cells to an ambient PM 0.1 —with or without cigarette smoke extract (CSE)—induced oxidative stress that activated the mitogen-activated protein kinases (MAPKs) to induce the pro-inflammatory cytokine IL-6 [31].…”

Section: Pathogenic Processes Implicated Following Inhalation Of Pmentioning

confidence: 99%

Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter

Traboulsi

Guerrina

et al. 2017

IJMS

141

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Air pollution of anthropogenic origin is largely from the combustion of biomass (e.g., wood), fossil fuels (e.g., cars and trucks), incinerators, landfills, agricultural activities and tobacco smoke. Air pollution is a complex mixture that varies in space and time, and contains hundreds of compounds including volatile organic compounds (e.g., benzene), metals, sulphur and nitrogen oxides, ozone and particulate matter (PM). PM0.1 (ultrafine particles (UFP)), those particles with a diameter less than 100 nm (includes nanoparticles (NP)) are considered especially dangerous to human health and may contribute significantly to the development of numerous respiratory and cardiovascular diseases such as chronic obstructive pulmonary disease (COPD) and atherosclerosis. Some of the pathogenic mechanisms through which PM0.1 may contribute to chronic disease is their ability to induce inflammation, oxidative stress and cell death by molecular mechanisms that include transcription factors such as nuclear factor κB (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Epigenetic mechanisms including non-coding RNA (ncRNA) may also contribute towards the development of chronic disease associated with exposure to PM0.1. This paper highlights emerging molecular concepts associated with inhalational exposure to PM0.1 and their ability to contribute to chronic respiratory and systemic disease.

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“…Our finding is in agreement with other reports showing accumulation of gold nanoparticles in lysosomes and extracellular vesicles following cellular uptake by phagocytosis can trigger TLR signaling pathway. 41–43 …”

Section: Discussionmentioning

confidence: 99%

Gold nanorods inhibit respiratory syncytial virus by stimulating the innate immune response

Bawage

Tiwari

Singh

et al. 2016

Nanomedicine: Nanotechnology, Biology and Medicine

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Respiratory syncytial virus (RSV) causes severe pneumonia and bronchiolitis in infants, children and older adults. The use of metallic nanoparticles as potential therapeutics is being explored against respiratory viruses like Influenza, Parainfluenza and Adenovirus. In this study, we showed that gold nanorods (GNRs) inhibit RSV in HEp-2 cells and BALB/c mice by 82% and 56%, respectively. The RSV inhibition correlated with marked upregulated antiviral genes due to GNR mediated TLR, NOD-like receptor and RIG-I-like receptor signaling pathways. Transmission electron microscopy of lungs showed GNRs in the endocytotic vesicles and histological analyses indicated infiltration by neutrophils, eosinophils and monocytes correlating with clearance of RSV. In addition, production of cytokines and chemokines in the lungs indicate recruitment of immune cells to counter RSV replication. To our knowledge, this is the first in vitro and in vivo report that provides possible antiviral mechanisms of GNRs against RSV.

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In vitro cytotoxicity of gold nanorods in A549 cells

Cited by 52 publications

References 31 publications

Oxidant-induced autophagy and ferritin degradation contribute to epithelial–mesenchymal transition through lysosomal iron

Oxidant-induced autophagy and ferritin degradation contribute to epithelial–mesenchymal transition through lysosomal iron

Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter

Gold nanorods inhibit respiratory syncytial virus by stimulating the innate immune response

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In vitro cytotoxicity of gold nanorods in A549 cells

Cited by 52 publications

References 31 publications

Oxidant-induced autophagy and ferritin degradation contribute to epithelial&ndash;mesenchymal transition through lysosomal iron

Oxidant-induced autophagy and ferritin degradation contribute to epithelial&ndash;mesenchymal transition through lysosomal iron

Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter

Gold nanorods inhibit respiratory syncytial virus by stimulating the innate immune response

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Oxidant-induced autophagy and ferritin degradation contribute to epithelial–mesenchymal transition through lysosomal iron

Oxidant-induced autophagy and ferritin degradation contribute to epithelial–mesenchymal transition through lysosomal iron