Inhibition of the WNT/β-catenin pathway by fine particulate matter in haze: Roles of metals and polycyclic aromatic hydrocarbons

Kang Yun Lee; Jun Ji Cao; Chii Hong Lee; Ta Chih Hsiao; Chi Tai Yeh; Thanh Tuan Huynh; Yong Ming Han; Xiang Dong Li; Kai Jen Chuang; Linwei Tian; Kin Fai Ho; Hsiao Chi Chuang

doi:10.1016/j.atmosenv.2015.03.017

Inhibition of the WNT/β-catenin pathway by fine particulate matter in haze: Roles of metals and polycyclic aromatic hydrocarbons

Kang Yun Lee, Jun Ji Cao, Chii Hong Lee, Ta Chih Hsiao, Chi Tai Yeh, Thanh Tuan Huynh, Yong Ming Han, Xiang Dong Li, Kai Jen Chuang, Linwei Tian, Kin Fai Ho, Hsiao Chi Chuang^*

^*Corresponding author for this work

Research output: Contribution to journal › Journal Article › peer-review

11 Scopus citations

Abstract

Air pollution might have a great impact on pulmonary health, but biological evidence in response to particulate matter less than 2.5μm in size (PM_2.5) has been lacking. Physicochemical characterization of haze PM_2.5 collected from Beijing, Xian and Hong Kong was performed. Biological pathways were identified by proteomic profiling in mouse lungs, suggesting that WNT/β-catenin is important in the response to haze PM_2.5. Suppression of β-catenin levels, activation of caspase-3 and alveolar destruction, as well as IL-6, TNF-α and IFN-γ production, were observed in the lungs. The inhibition of β-catenin, TCF4 and cyclin D1 was observed invitro in response to haze PM_2.5. The inhibition of WNT/β-catenin signaling, apoptosis-related results (caspase-3 and alveolar destruction), and inflammation, particularly including caspase-3 and alveolar destruction, were more highly associated with polycyclic aromatic hydrocarbons in haze PM_2.5. In conclusion, decreased WNT/β-catenin expression modulated by haze PM_2.5 could be involved in alveolar destruction and inflammation during haze episodes.

Original language	English
Pages (from-to)	118-129
Number of pages	12
Journal	Atmospheric Environment
Volume	109
DOIs	https://doi.org/10.1016/j.atmosenv.2015.03.017
State	Published - 01 05 2015
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2015 Elsevier Ltd.

Keywords

Air pollution
Apoptosis
Metal
Particulate matter
Polycyclic aromatic hydrocarbons
β-catenin

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10.1016/j.atmosenv.2015.03.017

Cite this

Lee, K. Y., Cao, J. J., Lee, C. H., Hsiao, T. C., Yeh, C. T., Huynh, T. T., Han, Y. M., Li, X. D., Chuang, K. J., Tian, L., Ho, K. F., & Chuang, H. C. (2015). Inhibition of the WNT/β-catenin pathway by fine particulate matter in haze: Roles of metals and polycyclic aromatic hydrocarbons. Atmospheric Environment, 109, 118-129. https://doi.org/10.1016/j.atmosenv.2015.03.017

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title = "Inhibition of the WNT/β-catenin pathway by fine particulate matter in haze: Roles of metals and polycyclic aromatic hydrocarbons",

abstract = "Air pollution might have a great impact on pulmonary health, but biological evidence in response to particulate matter less than 2.5μm in size (PM2.5) has been lacking. Physicochemical characterization of haze PM2.5 collected from Beijing, Xian and Hong Kong was performed. Biological pathways were identified by proteomic profiling in mouse lungs, suggesting that WNT/β-catenin is important in the response to haze PM2.5. Suppression of β-catenin levels, activation of caspase-3 and alveolar destruction, as well as IL-6, TNF-α and IFN-γ production, were observed in the lungs. The inhibition of β-catenin, TCF4 and cyclin D1 was observed invitro in response to haze PM2.5. The inhibition of WNT/β-catenin signaling, apoptosis-related results (caspase-3 and alveolar destruction), and inflammation, particularly including caspase-3 and alveolar destruction, were more highly associated with polycyclic aromatic hydrocarbons in haze PM2.5. In conclusion, decreased WNT/β-catenin expression modulated by haze PM2.5 could be involved in alveolar destruction and inflammation during haze episodes.",

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doi = "10.1016/j.atmosenv.2015.03.017",

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AU - Hsiao, Ta Chih

AU - Yeh, Chi Tai

AU - Huynh, Thanh Tuan

AU - Han, Yong Ming

AU - Li, Xiang Dong

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AU - Tian, Linwei

AU - Ho, Kin Fai

AU - Chuang, Hsiao Chi

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AB - Air pollution might have a great impact on pulmonary health, but biological evidence in response to particulate matter less than 2.5μm in size (PM2.5) has been lacking. Physicochemical characterization of haze PM2.5 collected from Beijing, Xian and Hong Kong was performed. Biological pathways were identified by proteomic profiling in mouse lungs, suggesting that WNT/β-catenin is important in the response to haze PM2.5. Suppression of β-catenin levels, activation of caspase-3 and alveolar destruction, as well as IL-6, TNF-α and IFN-γ production, were observed in the lungs. The inhibition of β-catenin, TCF4 and cyclin D1 was observed invitro in response to haze PM2.5. The inhibition of WNT/β-catenin signaling, apoptosis-related results (caspase-3 and alveolar destruction), and inflammation, particularly including caspase-3 and alveolar destruction, were more highly associated with polycyclic aromatic hydrocarbons in haze PM2.5. In conclusion, decreased WNT/β-catenin expression modulated by haze PM2.5 could be involved in alveolar destruction and inflammation during haze episodes.

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Inhibition of the WNT/β-catenin pathway by fine particulate matter in haze: Roles of metals and polycyclic aromatic hydrocarbons

Abstract

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Keywords

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