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Bisphenol A promotes X‐linked inhibitor of apoptosis protein‐dependent angiogenesis via G protein‐coupled estrogen receptor pathway
Author(s) -
Liu Jian,
Jin Xin,
Zhao Nana,
Ye Xiaolei,
Ying Chenjiang
Publication year - 2015
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3112
Subject(s) - xiap , angiogenesis , estrogen receptor , chemistry , nitric oxide , nitric oxide synthase , inhibitor of apoptosis , apoptosis , microbiology and biotechnology , signal transduction , receptor , estrogen receptor alpha , medicine , cancer research , endocrinology , biochemistry , biology , programmed cell death , cancer , caspase , organic chemistry , breast cancer
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 ERα or ERβ. Our data suggest that 100 n M 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 © 2015 John Wiley & Sons, Ltd.