Christiane Beer

Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro

Research output: Contribution to conferencePosterResearchpeer-review

Standard

Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro. / Foldbjerg, Rasmus; Beer, Christiane; Wang, Jing; Sutherland, Duncan S; Autrup, Herman.

2012. Poster session presented at Nanotoxicology 2012, Beijing, China.

Research output: Contribution to conferencePosterResearchpeer-review

Harvard

Foldbjerg, R, Beer, C, Wang, J, Sutherland, DS & Autrup, H 2012, 'Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro', Nanotoxicology 2012, Beijing, China, 04/09/2012 - 07/09/2012.

APA

Foldbjerg, R., Beer, C., Wang, J., Sutherland, D. S., & Autrup, H. (2012). Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro. Poster session presented at Nanotoxicology 2012, Beijing, China.

CBE

Foldbjerg R, Beer C, Wang J, Sutherland DS, Autrup H. 2012. Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro. Poster session presented at Nanotoxicology 2012, Beijing, China.

MLA

Foldbjerg, Rasmus et al. Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro. Nanotoxicology 2012, 04 Sep 2012, Beijing, China, Poster, 2012.

Vancouver

Foldbjerg R, Beer C, Wang J, Sutherland DS, Autrup H. Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro. 2012. Poster session presented at Nanotoxicology 2012, Beijing, China.

Author

Bibtex

@conference{3a605c54c9914cdf95f84403858e8bc3,
title = "Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro",
abstract = "Much of the concerns regarding engineered NP toxicity are based on knowledge from previous studies on ambient and environmental particles. E.g., the effects of exposure to silica dust particles have been studied intensively due to the carcinogenicity of crystalline silica. However, the increasing usage of engineered amorphous silica NPs has emphasized the need for further mechanistic insight to predict the consequences of exposure to the amorphous type of silica NPs. Recently, the parallelogram approach was proposed as a scheme to assess biological effects of nanomaterials (Krug and Wick, 2011). Accordingly, the present study focused on the cytotoxicity of amorphous silica NPs in six different cell lines selected to explore the significance of tissue type and species. The cells were selected as three pairs of human/mouse cell lines derived from lung epithelium (A549 and ASB-XIV), colon epithelium (CaCo-2 and Colon-26) and macrophages (THP-1 and J774A.1).Viability data demonstrated that macrophages were most sensitive to silica NP and interestingly, murine cell lines were generally found to be more sensitive than comparable human cell lines. Further studies were conducted in the human epithelial lung cell line, A549, to investigate the mechanism of action. A concentration-dependent increase of cellular reactive oxygen species was demonstrated in silica NP exposed A549 cells. However, induction of oxidative stress related pathways was not found after silica NP exposure in gene array studies on global gene expression. Instead, up-regulated genes primarily related to lipid metabolism and biosynthesis whereas down-regulated genes were enriched in several processes, including transcription, cell junction and extra cellular matrix (ECM)-receptor interaction. Accordingly, our data suggest that oxidative stress might not be the main mediator of amorphous silica NP toxicity. Furthermore, the differential response in different cell lines suggests careful consideration in the choice of cell models and cautions that interspecies extrapolation may have to consider higher sensitivity in mice towards NPs.",
author = "Rasmus Foldbjerg and Christiane Beer and Jing Wang and Sutherland, {Duncan S} and Herman Autrup",
year = "2012",
month = sep,
language = "English",
note = "null ; Conference date: 04-09-2012 Through 07-09-2012",

}

RIS

TY - CONF

T1 - Cellular effects and gene expression after exposure to amorphous silica nanoparticles in vitro

AU - Foldbjerg, Rasmus

AU - Beer, Christiane

AU - Wang, Jing

AU - Sutherland, Duncan S

AU - Autrup, Herman

PY - 2012/9

Y1 - 2012/9

N2 - Much of the concerns regarding engineered NP toxicity are based on knowledge from previous studies on ambient and environmental particles. E.g., the effects of exposure to silica dust particles have been studied intensively due to the carcinogenicity of crystalline silica. However, the increasing usage of engineered amorphous silica NPs has emphasized the need for further mechanistic insight to predict the consequences of exposure to the amorphous type of silica NPs. Recently, the parallelogram approach was proposed as a scheme to assess biological effects of nanomaterials (Krug and Wick, 2011). Accordingly, the present study focused on the cytotoxicity of amorphous silica NPs in six different cell lines selected to explore the significance of tissue type and species. The cells were selected as three pairs of human/mouse cell lines derived from lung epithelium (A549 and ASB-XIV), colon epithelium (CaCo-2 and Colon-26) and macrophages (THP-1 and J774A.1).Viability data demonstrated that macrophages were most sensitive to silica NP and interestingly, murine cell lines were generally found to be more sensitive than comparable human cell lines. Further studies were conducted in the human epithelial lung cell line, A549, to investigate the mechanism of action. A concentration-dependent increase of cellular reactive oxygen species was demonstrated in silica NP exposed A549 cells. However, induction of oxidative stress related pathways was not found after silica NP exposure in gene array studies on global gene expression. Instead, up-regulated genes primarily related to lipid metabolism and biosynthesis whereas down-regulated genes were enriched in several processes, including transcription, cell junction and extra cellular matrix (ECM)-receptor interaction. Accordingly, our data suggest that oxidative stress might not be the main mediator of amorphous silica NP toxicity. Furthermore, the differential response in different cell lines suggests careful consideration in the choice of cell models and cautions that interspecies extrapolation may have to consider higher sensitivity in mice towards NPs.

AB - Much of the concerns regarding engineered NP toxicity are based on knowledge from previous studies on ambient and environmental particles. E.g., the effects of exposure to silica dust particles have been studied intensively due to the carcinogenicity of crystalline silica. However, the increasing usage of engineered amorphous silica NPs has emphasized the need for further mechanistic insight to predict the consequences of exposure to the amorphous type of silica NPs. Recently, the parallelogram approach was proposed as a scheme to assess biological effects of nanomaterials (Krug and Wick, 2011). Accordingly, the present study focused on the cytotoxicity of amorphous silica NPs in six different cell lines selected to explore the significance of tissue type and species. The cells were selected as three pairs of human/mouse cell lines derived from lung epithelium (A549 and ASB-XIV), colon epithelium (CaCo-2 and Colon-26) and macrophages (THP-1 and J774A.1).Viability data demonstrated that macrophages were most sensitive to silica NP and interestingly, murine cell lines were generally found to be more sensitive than comparable human cell lines. Further studies were conducted in the human epithelial lung cell line, A549, to investigate the mechanism of action. A concentration-dependent increase of cellular reactive oxygen species was demonstrated in silica NP exposed A549 cells. However, induction of oxidative stress related pathways was not found after silica NP exposure in gene array studies on global gene expression. Instead, up-regulated genes primarily related to lipid metabolism and biosynthesis whereas down-regulated genes were enriched in several processes, including transcription, cell junction and extra cellular matrix (ECM)-receptor interaction. Accordingly, our data suggest that oxidative stress might not be the main mediator of amorphous silica NP toxicity. Furthermore, the differential response in different cell lines suggests careful consideration in the choice of cell models and cautions that interspecies extrapolation may have to consider higher sensitivity in mice towards NPs.

M3 - Poster

Y2 - 4 September 2012 through 7 September 2012

ER -