Effects of silver nanoparticles on the interactions of neuron- and glia-like cells

Toxicity, uptake mechanisms, and lysosomal tracking

I. Lun Hsiao, Yi Kong Hsieh, Chun Yu Chuang, Chu Fang Wang, Yuh Jeen Huang

研究成果: 雜誌貢獻文章

18 引文 (Scopus)

摘要

Silver nanoparticles (AgNPs) are commonly used nanomaterials in consumer products. Previous studies focused on its effects on neurons; however, little is known about their effects and uptake mechanisms on glial cells under normal or activated states. Here, ALT astrocyte-like, BV-2 microglia and differentiated N2a neuroblastoma cells were directly or indirectly exposed to 10 nm AgNPs using mono- and co-culture system. A lipopolysaccharide (LPS) was pretreated to activate glial cells before AgNP treatment for mimicking NP exposure under brain inflammation. From mono-culture, ALT took up the most AgNPs and had the lowest cell viability within three cells. Moreover, AgNPs induced H2O2 and NO from ALT/activated ALT and BV-2, respectively. However, AgNPs did not induce cytokines release (IL-6, TNF-α, MCP-1). LPS-activated BV-2 took up more AgNPs than normal BV-2, while the induction of ROS and cytokines from activated cells were diminished. Ca2+-regulated clathrin- and caveolae-independent endocytosis and phagocytosis were involved in the AgNP uptake in ALT, which caused more rapid NP translocation to lysosome than in macropinocytosis and clathrin-dependent endocytosis-involved BV-2. AgNPs directly caused apoptosis and necrosis in N2a cells, while by indirect NP exposure to bottom chamber ALT or BV-2 in Transwell, more apoptotic upper chamber N2a cells were observed. Cell viability of BV-2 also decreased in an ALT–BV-2 co-culturing study. The damaged cells correlated to NP-mediated H2O2 release from ALT or NO from BV-2, which indicates that toxic response of AgNPs to neurons is not direct, but indirectly arises from AgNP-induced soluble factors from other glial cells.
原文英語
頁(從 - 到)1742-1753
頁數12
期刊Environmental Toxicology
32
發行號6
DOIs
出版狀態已發佈 - 六月 1 2017
對外發佈Yes

指紋

Silver
Neuroglia
Nanoparticles
Neurons
Toxicity
silver
Clathrin
viability
toxicity
Lipopolysaccharides
apoptosis
monoculture
Cells
translocation
Cytokines
brain
Consumer products
Poisons
Endocytosis
Nanostructured materials

ASJC Scopus subject areas

  • Toxicology
  • Management, Monitoring, Policy and Law
  • Health, Toxicology and Mutagenesis

引用此文

Effects of silver nanoparticles on the interactions of neuron- and glia-like cells : Toxicity, uptake mechanisms, and lysosomal tracking. / Hsiao, I. Lun; Hsieh, Yi Kong; Chuang, Chun Yu; Wang, Chu Fang; Huang, Yuh Jeen.

於: Environmental Toxicology, 卷 32, 編號 6, 01.06.2017, p. 1742-1753.

研究成果: 雜誌貢獻文章

Hsiao, I. Lun ; Hsieh, Yi Kong ; Chuang, Chun Yu ; Wang, Chu Fang ; Huang, Yuh Jeen. / Effects of silver nanoparticles on the interactions of neuron- and glia-like cells : Toxicity, uptake mechanisms, and lysosomal tracking. 於: Environmental Toxicology. 2017 ; 卷 32, 編號 6. 頁 1742-1753.
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AU - Hsieh, Yi Kong

AU - Chuang, Chun Yu

AU - Wang, Chu Fang

AU - Huang, Yuh Jeen

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AB - Silver nanoparticles (AgNPs) are commonly used nanomaterials in consumer products. Previous studies focused on its effects on neurons; however, little is known about their effects and uptake mechanisms on glial cells under normal or activated states. Here, ALT astrocyte-like, BV-2 microglia and differentiated N2a neuroblastoma cells were directly or indirectly exposed to 10 nm AgNPs using mono- and co-culture system. A lipopolysaccharide (LPS) was pretreated to activate glial cells before AgNP treatment for mimicking NP exposure under brain inflammation. From mono-culture, ALT took up the most AgNPs and had the lowest cell viability within three cells. Moreover, AgNPs induced H2O2 and NO from ALT/activated ALT and BV-2, respectively. However, AgNPs did not induce cytokines release (IL-6, TNF-α, MCP-1). LPS-activated BV-2 took up more AgNPs than normal BV-2, while the induction of ROS and cytokines from activated cells were diminished. Ca2+-regulated clathrin- and caveolae-independent endocytosis and phagocytosis were involved in the AgNP uptake in ALT, which caused more rapid NP translocation to lysosome than in macropinocytosis and clathrin-dependent endocytosis-involved BV-2. AgNPs directly caused apoptosis and necrosis in N2a cells, while by indirect NP exposure to bottom chamber ALT or BV-2 in Transwell, more apoptotic upper chamber N2a cells were observed. Cell viability of BV-2 also decreased in an ALT–BV-2 co-culturing study. The damaged cells correlated to NP-mediated H2O2 release from ALT or NO from BV-2, which indicates that toxic response of AgNPs to neurons is not direct, but indirectly arises from AgNP-induced soluble factors from other glial cells.

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