Indirect effects of TiO2 nanoparticle on neuron-glial cell interactions

I. Lun Hsiao, Chia Cheng Chang, Chung Yi Wu, Yi Kong Hsieh, Chun Yu Chuang, Chu Fang Wang, Yuh Jeen Huang

研究成果: 雜誌貢獻文章

13 引文 (Scopus)

摘要

Although, titanium dioxide nanoparticles (TiO2NPs) are nanomaterials commonly used in consumer products, little is known about their hazardous effects, especially on central nervous systems. To examine this issue, ALT astrocyte-like, BV-2 microglia and differentiated N2a neuroblastoma cells were exposed to 6 nm of 100% anatase TiO2NPs. A lipopolysaccharide (LPS) was pre-treated to activate glial cells before NP treatment for mimicking NP exposure under brain injury. We found that ALT and BV-2 cells took up more NPs than N2a cells and caused lower cell viability. TiO2NPs induced IL-1β in the three cell lines and IL-6 in N2a. LPS-activated BV-2 took up more TiO2NPs than normal BV-2 and released more intra/extracellular reactive oxygen species (ROS), IL-1β, IL-6 and MCP-1 than did activated BV-2. Involvement of clathrin- and caveolae-dependent endocytosis in ALT and clathrin-dependent endocytosis and phagocytosis in BV-2 both had a slow NP translocation rate to lysosome, which may cause slow ROS production (after 24 h). Although TiO2NPs did not directly cause N2a viability loss, by indirect NP exposure to the bottom chamber of LPS-activated BV-2 in the Transwell system, they caused late apoptosis and loss of cell viability in the upper N2a chamber due to H2O2 and/or TNF-α release from BV-2. However, none of the adverse effects in N2a or BV-2 cells was observed when TiO2NPs were exposed to ALT-N2a or ALT-BV-2 co-culture. These results demonstrate that neuron damage can result from TiO2NP-mediated ROS and/or cytokines release from microglia, but not from astrocytes.
原文英語
頁(從 - 到)34-44
頁數11
期刊Chemico-Biological Interactions
254
DOIs
出版狀態已發佈 - 七月 25 2016
對外發佈Yes

指紋

Cell Communication
Neuroglia
Nanoparticles
Neurons
Lipopolysaccharides
Reactive Oxygen Species
Clathrin
Cells
Interleukin-1
Interleukin-6
Microglia
Endocytosis
Astrocytes
Cell Survival
Consumer products
Neurology
Nanostructured materials
Caveolae
Nanostructures
Brain

ASJC Scopus subject areas

  • Toxicology

引用此文

Hsiao, I. L., Chang, C. C., Wu, C. Y., Hsieh, Y. K., Chuang, C. Y., Wang, C. F., & Huang, Y. J. (2016). Indirect effects of TiO2 nanoparticle on neuron-glial cell interactions. Chemico-Biological Interactions, 254, 34-44. https://doi.org/10.1016/j.cbi.2016.05.024

Indirect effects of TiO2 nanoparticle on neuron-glial cell interactions. / Hsiao, I. Lun; Chang, Chia Cheng; Wu, Chung Yi; Hsieh, Yi Kong; Chuang, Chun Yu; Wang, Chu Fang; Huang, Yuh Jeen.

於: Chemico-Biological Interactions, 卷 254, 25.07.2016, p. 34-44.

研究成果: 雜誌貢獻文章

Hsiao, I. Lun ; Chang, Chia Cheng ; Wu, Chung Yi ; Hsieh, Yi Kong ; Chuang, Chun Yu ; Wang, Chu Fang ; Huang, Yuh Jeen. / Indirect effects of TiO2 nanoparticle on neuron-glial cell interactions. 於: Chemico-Biological Interactions. 2016 ; 卷 254. 頁 34-44.
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AU - Chuang, Chun Yu

AU - Wang, Chu Fang

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AB - Although, titanium dioxide nanoparticles (TiO2NPs) are nanomaterials commonly used in consumer products, little is known about their hazardous effects, especially on central nervous systems. To examine this issue, ALT astrocyte-like, BV-2 microglia and differentiated N2a neuroblastoma cells were exposed to 6 nm of 100% anatase TiO2NPs. A lipopolysaccharide (LPS) was pre-treated to activate glial cells before NP treatment for mimicking NP exposure under brain injury. We found that ALT and BV-2 cells took up more NPs than N2a cells and caused lower cell viability. TiO2NPs induced IL-1β in the three cell lines and IL-6 in N2a. LPS-activated BV-2 took up more TiO2NPs than normal BV-2 and released more intra/extracellular reactive oxygen species (ROS), IL-1β, IL-6 and MCP-1 than did activated BV-2. Involvement of clathrin- and caveolae-dependent endocytosis in ALT and clathrin-dependent endocytosis and phagocytosis in BV-2 both had a slow NP translocation rate to lysosome, which may cause slow ROS production (after 24 h). Although TiO2NPs did not directly cause N2a viability loss, by indirect NP exposure to the bottom chamber of LPS-activated BV-2 in the Transwell system, they caused late apoptosis and loss of cell viability in the upper N2a chamber due to H2O2 and/or TNF-α release from BV-2. However, none of the adverse effects in N2a or BV-2 cells was observed when TiO2NPs were exposed to ALT-N2a or ALT-BV-2 co-culture. These results demonstrate that neuron damage can result from TiO2NP-mediated ROS and/or cytokines release from microglia, but not from astrocytes.

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