MPA-modified CdTe quantum dots increased interleukin-1beta secretion through MyD88-dependent Toll-like receptor pathway and NLRP3 inflammasome activation in microglia

Wu, Tianshu; Li, Xue; He, Keyu; Wei, Tingting; Wang, Yan; Lu, Jie; Ying, Yao; Zhang, Ting; Yang, Xue; Tang, Meng

doi:10.1016/j.tiv.2018.05.014

Cited by 29 publications

(20 citation statements)

References 44 publications

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“…46 A few available data concerning cytotoxic properties of CdTeQDs toward microglial cells also confirm our results. Wu et al 47 reported only 20% loss of viability of BV-2 cells treated with 30 nM CdTeQDs, and similar results were obtained for rat microglial N9 cells. 32 In contrast, CeO 2 NPs, although used at a relatively high concentration (100 µg/mL), did not affect BV-2 cell viability (Figure 4).…”

Section: Discussionsupporting

confidence: 60%

“…Despite the well-documented toxicity of CdTeQDs, there are not many studies concerning their effects of on cytokine release by mammalian cells. Wu et al 47 observed an increased release of IL-1 β mRNA and protein in BV-2 cells after treatment with 3-mercaptopropionic acid (MPA)-modified CdTeQDs (40 nM). Interestingly, an increase in mRNA level of IFN α and TNF α was also reported, however, without any mention about protein release.…”

Section: Discussionmentioning

confidence: 99%

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Diminished amyloid-β uptake by mouse microglia upon treatment with quantum dots, silver or cerium oxide nanoparticles: Nanoparticles and amyloid-β uptake by microglia

et al. 2019

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Alzheimer’s disease (AD) is a chronic neurodegenerative disease leading to progressive dementia in elderly people. The disease is characterized, among others, by formation of amyloid- β (A β) polypeptide plaques in the brain. Although etiology of the disease is not fully understood, recent research suggest that nanomaterials may affect AD development. Here, we described the consequences of exposure of mouse BV-2 microglia to silver nanoparticles (AgNPs, 50 µg/mL), cerium oxide nanoparticles (CeO2NPs, 100 µg/mL), and cadmium telluride quantum dots (CdTeQDs, 3 or 10 µg/mL) in the context of its ability to clear A β plaques. The brain microglial cells play an important role in removing A β plaques from the brain. Cell viability and cycle progression were assessed by trypan blue test and propidium iodide binding, respectively. The uptake of A β and NPs was measured by flow cytometry. Secretion of proinflammatory cytokines was measured with the use of cytometric bead array. A β (0.1 μM) did not affect viability, whereas NPs decreased microglia growth by arresting the cells in G1 phase (CdTeQDs) or in S phase (AgNPs and CeO2NPs) of cell cycle. The uptake of A β was significantly reduced in the presence of AgNPs and CeO2NPs. In addition, the least toxic CeO2NPs induced the release of proinflammatory cytokine, tumor necrosis factor α. In summary, each of the NPs tested affected either the microglia phagocytic activity (AgNPs and CeO2NPs) and/or its viability (AgNPs and CdTeQDs) that may favor the occurrence of AD and accelerate its development.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Diminished amyloid-β uptake by mouse microglia upon treatment with quantum dots, silver or cerium oxide nanoparticles: Nanoparticles and amyloid-β uptake by microglia

et al. 2019

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“…Total protein of BV2 cells was extracted to do western blotting analysis, which was carried out following the protocol described in a previous study [ 57 ]. The same samples were ran three times and the experiment was repeated independently at least three times.…”

Section: Methodsmentioning

confidence: 99%

Induction of ferroptosis in response to graphene quantum dots through mitochondrial oxidative stress in microglia

Liu

et al. 2020

Part Fibre Toxicol

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Background Graphene quantum dots (GQDs) provide a bright prospect in the biomedical application because they contain low-toxic compounds and promise imaging of deep tissues and tiny vascular structures. However, the biosafety of this novel QDs has not been thoroughly evaluated, especially in the central nervous system (CNS). The microarray analysis provides a hint that nitrogen-doped GQDs (N-GQDs) exposure could cause ferroptosis in microglia, which is a novel form of cell death dependent on iron overload and lipid peroxidation. Results The cytosolic iron overload, glutathione (GSH) depletion, excessive reactive oxygen species (ROS) production and lipid peroxidation (LPO) were observed in microglial BV2 cells treated with N-GQDs, which indicated that N-GQDs could damage the iron metabolism and redox balance in microglia. The pre-treatments of a specific ferroptosis inhibitor Ferrostatin-1 (Fer-1) and an iron chelater Deferoxamine mesylate (DFO) not only inhibited cell death, but also alleviated iron overload, LPO and alternations in ferroptosis biomarkers in microglia, which were caused by N-GQDs. When assessing the potential mechanisms of N-GQDs causing ferroptosis in microglia, we found that the iron content, ROS generation and LPO level in mitochondria of BV2 cells all enhanced after N-GQDs exposure. When the antioxidant ability of mitochondria was increased by the pre-treatment of a mitochondria targeted ROS scavenger MitoTEMPO, the ferroptotic biological changes were effectively reversed in BV2 cells treated with N-GQDs, which indicated that the N-GQDs-induced ferroptosis in microglia could be attributed to the mitochondrial oxidative stress. Additionally, amino functionalized GQDs (A-GQDs) elicited milder redox imbalance in mitochondria and resulted in less ferroptotic effects than N-GQDs in microglia, which suggested a slight protection of amino group functionalization in GQDs causing ferroptosis. Conclusion N-GQDs exposure caused ferroptosis in microglia via inducing mitochondrial oxidative stress, and the ferroptotic effects induced by A-GQDs were milder than N-GQDs when the exposure method is same. This study will not only provide new insights in the GQDs-induced cell damage performed in multiple types of cell death, but also in the influence of chemical modification on the toxicity of GQDs.

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“…According to our recent study, CdTe QDs were able to polarize BV‐2 cells from a homeostatic status to an M1 phenotype, based on the increased expressions of the cell surface antigens CD11b and CD40. At the same time, increases in interferon‐α, tumor necrosis factor‐α, and interleukin‐1β were confirmed by quantitative reverse transcription‐polymerase chain reaction and enzyme‐linked immunosorbent assays (Wu et al, ).…”

Section: Introductionmentioning

confidence: 93%

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

Wei

et al. 2018

J of Applied Toxicology

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Microglial cells are resident immune cells in the central nervous system. Activation of microglia as induced by CdTe quantum dots (QDs) can trigger damage to neurons. To quantify the intracellular QDs, we monitored the intracellular Cd concentration in the QD‐exposed mouse microglial cells (BV‐2 cell line). The extent of cell injury at different times correlated with the Cd concentration in cells at that time. In addition to Cd ion detection, we also monitored the intracellular fluorescence of the QDs. More QDs accumulated in the nucleus than in the cytoplasm. Comet assays confirmed that QDs induce DNA damage. However, DNA cannot interact with QDs, so the DNA damage was not caused by CdTe QDs adducts to DNA but by the increase of the Cd ion concentration and the secondary oxidative damage. In addition to DNA damage, biofilm injury and endogenous reduced glutathione depletion were also apparent in QD‐exposed BV‐2 cells. These changes can be prevented or even reversed by exogenous reduced glutathione administration.

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MPA-modified CdTe quantum dots increased interleukin-1beta secretion through MyD88-dependent Toll-like receptor pathway and NLRP3 inflammasome activation in microglia

Cited by 29 publications

References 44 publications

Diminished amyloid-β uptake by mouse microglia upon treatment with quantum dots, silver or cerium oxide nanoparticles: Nanoparticles and amyloid-β uptake by microglia

Diminished amyloid-β uptake by mouse microglia upon treatment with quantum dots, silver or cerium oxide nanoparticles: Nanoparticles and amyloid-β uptake by microglia

Induction of ferroptosis in response to graphene quantum dots through mitochondrial oxidative stress in microglia

DNA damage in BV‐2 cells: An important supplement to the neurotoxicity of CdTe quantum dots

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