RCEES OpenIR  > 环境化学与生态毒理学国家重点实验室
HIF-1alpha/VEGF pathway mediates 1,3,6,8-tetrabromo-9 H-carbazole-induced angiogenesis: a potential vascular toxicity of an emerging contaminant
Xu, Tong; Hu, Xiaoxu; Yang, Guanglei; Liu, Yiyun; Zhang, Qian; Yu, Shuyuan; Chen, Guomin; Li, Yunping; Sha, Rui; Chen, Yangsheng; Xie, Heidi Qunhui; Guo, Tai L.; Xu, Li; Zhao, Bin
2022-06-15
Source PublicationJOURNAL OF HAZARDOUS MATERIALS
ISSN0304-3894
Volume432Issue:0Pages:128718
AbstractThe dioxin-like substances polyhalogenated carbazoles (PHCZs) may trigger the aryl hydrocarbon receptor (AhR) signaling pathway. Although the crosstalk between AhR and the hypoxia inducible factor-1 (HIF-1) pathways is generally believed to occur, the exact mechanisms of the HIF-1 pathway in PHCZ toxicity have not been determined. We aimed to elucidate the effect of PHCZs on the HIF-1 pathway and its involvement in the regulation of target genes of HIF-1. Herein, we employed human HepG2 cells transiently transfected with a hypoxia response element (HRE) luciferase reporter to identify PHCZs that could influence HIF-1 pathway. We found that exposure to one of the four selected PHCZs, specifically 1,3,6,8-tetrabromo-9 H-carbazole (1368-BCZ), induced a significant enhancement of the activity of HRE activity. In silico data supported 1368-BCZ-induced HIF-1 alpha activity preferentially. Moreover, 1368-BCZ significantly upregulated the expression of HIF-1 target genes, including endothelial growth factor (VEGF) and erythropoietin. Importantly, the stimulated secretion of VEGF by 1368-BCZ promoted the angiogenesis in human umbilical vein endothelial cells. Therefore, the present
Department环境化学与生态毒理学国家重点实验室 ; 环境化学与生态毒理学国家重点实验室
KeywordARYL-HYDROCARBON RECEPTOR HALOGENATED CARBAZOLES TUMOR ANGIOGENESIS HYPOXIA DIOXIN VEGF HIF-1-ALPHA SYSTEM CANCER OXYGEN
Document Type期刊论文
Identifierhttps://ir.rcees.ac.cn/handle/311016/47544
Collection环境化学与生态毒理学国家重点实验室
Corresponding AuthorXu, Li
Affiliation1.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
2.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
3.Beijing Hosp, Natl Ctr Gerontol, Dept Cardiol, Beijing 100730, Peoples R China
4.Shenzhen Ctr Dis Control & Prevent, Environm & Hlth Dept, Shenzhen 518055, Guangdong, Peoples R China
5.Univ Chinese Acad Sci, Sch Environm, Hangzhou Inst Adv Study, Hangzhou 310024, Peoples R China
Recommended Citation
GB/T 7714
Xu, Tong,Hu, Xiaoxu,Yang, Guanglei,et al. HIF-1alpha/VEGF pathway mediates 1,3,6,8-tetrabromo-9 H-carbazole-induced angiogenesis: a potential vascular toxicity of an emerging contaminant[J]. JOURNAL OF HAZARDOUS MATERIALS,2022,432(0):128718.
APA Xu, Tong.,Hu, Xiaoxu.,Yang, Guanglei.,Liu, Yiyun.,Zhang, Qian.,...&Zhao, Bin.(2022).HIF-1alpha/VEGF pathway mediates 1,3,6,8-tetrabromo-9 H-carbazole-induced angiogenesis: a potential vascular toxicity of an emerging contaminant.JOURNAL OF HAZARDOUS MATERIALS,432(0),128718.
MLA Xu, Tong,et al."HIF-1alpha/VEGF pathway mediates 1,3,6,8-tetrabromo-9 H-carbazole-induced angiogenesis: a potential vascular toxicity of an emerging contaminant".JOURNAL OF HAZARDOUS MATERIALS 432.0(2022):128718.
Files in This Item: Download All
File Name/Size DocType Version Access License
HIF-1alpha_VEGF path(3729KB)期刊论文出版稿开放获取CC BY-NC-SAView Download
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Xu, Tong]'s Articles
[Hu, Xiaoxu]'s Articles
[Yang, Guanglei]'s Articles
Baidu academic
Similar articles in Baidu academic
[Xu, Tong]'s Articles
[Hu, Xiaoxu]'s Articles
[Yang, Guanglei]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Xu, Tong]'s Articles
[Hu, Xiaoxu]'s Articles
[Yang, Guanglei]'s Articles
Terms of Use
No data!
Social Bookmark/Share
File name: HIF-1alpha_VEGF pathway mediates 1,3,6,8-tetrabromo-9 H-carbazole-induced angiogenesis_ a potential vascular toxicity of an emerging contaminant.pdf
Format: Adobe PDF
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.