Bisphenol A promotes X-linked inhibitor of apoptosis protein-dependent angiogenesis via G protein-coupled estrogen receptor pathway

被引:13
作者
Liu, Jian [1 ,2 ]
Jin, Xin [1 ]
Zhao, Nana [3 ]
Ye, Xiaolei [3 ]
Ying, Chenjiang [1 ,4 ]
机构
[1] Huazhong Univ Sci & Technol, Dept Food Hyg & Nutr, Sch Publ Hlth, Tongji Med Coll, Wuhan 430030, Hubei, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Pediat, Zhengzhou 450052, Peoples R China
[3] Wenzhou Med Univ, Sch Environm Sci & Publ Hlth, Wenzhou, Peoples R China
[4] Huazhong Univ Sci & Technol, MOE Key Lab Environm & Hlth, Sch Publ Hlth, Tongji Med Coll, Wuhan 430030, Hubei, Peoples R China
关键词
Bisphenol A; Angiogenesis; X-linked inhibitor of apoptosis protein; G protein-coupled estrogen receptor; Caveolin-1; WIDESPREAD EXPOSURE; BREAST-CANCER; MECHANISMS; GPR30; INDUCTION; SURVIVAL; XIAP; IAPS;
D O I
10.1002/jat.3112
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 [卫生毒理学];
摘要
Bisphenol A (BPA), one of the high-volume chemicals worldwide, has a core structure resembling that of natural estradiol. Recent evidence has demonstrated that exposure to BPA has a relationship with the risk of cancer. The objective of our study is to investigate the mechanisms underlying the pro-angiogenic effects of BPA. We demonstrated that BPA markedly induces endothelial cell proliferation, migration and tube formation by activating endothelial nitric oxide synthase. BPA-induced nitric oxide generation appeared to be associated with the X-linked inhibitor of apoptosis protein (XIAP), which competes with endothelial nitric oxide synthase for caveolin-1. BPA was shown to exert its pro-angiogenic effect by upregulating XIAP expression via G protein-coupled estrogen receptor (ER) activation but not via ER or ER. Our data suggest that 100nM BPA promote angiogenesis in a G protein-coupled ER-dependent genomic pathway, and provide a novel insight into the potential role of XIAP in mediating the pro-angiogenic effects of BPA in endothelial cells. Copyright (c) 2015 John Wiley & Sons, Ltd. Our study investigates the mechanisms underlying the pro-angiogenic effects of bisphenol A (BPA). We demonstrated that BPA markedly induces endothelial cell proliferation, migration and tube formation by activating endothelial nitric oxide synthase. BPA-induced nitric oxide generation appeared to be associated with X-linked inhibitor of apoptosis protein, which competes with endothelial nitric oxide synthase for caveolin-1. BPA was shown to exert its pro-angiogenic effect by upregulating X-linked inhibitor of apoptosis protein expression via G protein-coupled estrogen receptor activation but not via estrogen receptor ER or ER.
引用
收藏
页码:1309 / 1317
页数:9
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