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Inhibition of the WNT/b-catenin pathway by fine particulate matter inhaze: Roles of metals and polycyclic aromatic hydrocarbons
Lee,KY(Lee,Kang-Yun)[1,2]; Cao,JJ(Cao,Junji)[3]; Lee,CH(Lee,Chii-Hong)[4]; Hsiao,T-C(Hsiao,Ta-Chih)[5]; Yeh,C-T(Yeh,Chi-Tai)[6]; Huynh,T-T(Huynh,Thanh-Tuan)[7]; Han,YM(Han,Yongming)[3]; Li,XD(Li,Xiangdong)[8]; Chuang,KJ(Chuang,Kai-Jen)[9,10]; Tian,LW(Tian,Linwei)[11]; Ho,KF(Ho,Kin-Fai)[12,13]; Chuang,H-C(Chuang,Hsiao-Chi)[1,14]
2015-05
发表期刊Atmospheric Environment
卷号109期号:2015页码:118-129
文章类型期刊论文
摘要

Air pollution might have a great impact on pulmonary health, but biological evidence in response to particulate matter less than 2.5 μm 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 in vitro 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.

关键词Air Pollution Apoptosis B-catenin Metal Particulate Matter Polycyclic Aromatic Hydrocarbons
DOI10.1016/j.atmosenv.2015.03.017
收录类别SCI
语种英语
引用统计
文献类型期刊论文
条目标识符http://ir.ieecas.cn/handle/361006/9477
专题粉尘与环境研究室
作者单位1.Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan;
2.Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;
3.Key Laboratory of Aerosol, SKLLQG, Institute of Earth Environment, Chinese Academy of Sciences, Xi'an 710075, China;
4.Department of Pathology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan;
5.Graduate Institute of Environmental Engineering, National Central University, Taoyuan, Taiwan;
6.Cancer Center, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan;
7.Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;
8.Department of the Civil and Environmental Engineering, The Hong Kong Polytechnic University, Kowloon, Hong Kong;
9.Department of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;
10.School of Public Health, College of Public Health and Nutrition, Taipei Medical University, Taipei, Taiwan;
11.School of Public Health, The University of Hong Kong, Hong Kong SAR, China;
12.Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong;
13.Shenzhen Municipal Key Laboratory for Health Risk Analysis, Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, China;
14.School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan
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GB/T 7714
Lee,KY,Cao,JJ,Lee,CH,et al. Inhibition of the WNT/b-catenin pathway by fine particulate matter inhaze: Roles of metals and polycyclic aromatic hydrocarbons[J]. Atmospheric Environment,2015,109(2015):118-129.
APA Lee,KY.,Cao,JJ.,Lee,CH.,Hsiao,T-C.,Yeh,C-T.,...&Chuang,H-C.(2015).Inhibition of the WNT/b-catenin pathway by fine particulate matter inhaze: Roles of metals and polycyclic aromatic hydrocarbons.Atmospheric Environment,109(2015),118-129.
MLA Lee,KY,et al."Inhibition of the WNT/b-catenin pathway by fine particulate matter inhaze: Roles of metals and polycyclic aromatic hydrocarbons".Atmospheric Environment 109.2015(2015):118-129.
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