Exposure to environmental bisphenol A inhibits HTR-8/SVneo cell migration and invasion
Pu Wei1
Dongqing Ru2
Xiaoqian Li2
Dongyan Shi2
Mingshun Zhang2
Qing Xu3
Hong Zhou4
Shuang Wen2
1.Department of Immunology, Nanjing Medical University, Nanjing, Jiangsu 211166, China;Department of Obstetrics, the Affiliated Hangzhou Hospital of Nanjing Medical University, Hangzhou, Zhejiang 310006, China2.Department of Immunology, Nanjing Medical University, Nanjing, Jiangsu 211166, China3.Department of Gynecology, the Affiliated Obstetrics and Gynecology Hospital of Nanjing Medical University, Nanjing, Jiangsu 210004, China4.Department of Immunology, Nanjing Medical University, Nanjing, Jiangsu 211166, China;Department of Biotherapy, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210011, China
摘要：Environmental pollutants,such as bisphenol A (BPA) have recently been implicated in the development of adverse birth outcomes.However,the underlying teratogenic mechanisms remain unclear.We investigated the effects of BPA on the migration and invasion of human primary extravillous trophoblast HTR-8/SVneo cells.Our results indicated that BPA reduced cell migration and invasion.Moreover,it altered the ratio of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) by downregulating MMP-2 and MMP-9,and upregulating TIMP-1 and TIMP-2.Furthermore,BPA suppressed integrin β1,integrin α5,and vimentin.Interestingly,BPA-induced invasion was partially restored by G15,a membrane G-protein-coupled estrogen receptor 30 antagonist.We further revealed that 42 proteins were differentially expressed by mass spectrometry analysis,which could be divided into three categories based on gene ontology including biological process,cellular component,and molecular function.These results suggest that BPA reduces HTR-8/SVneo cell migration and invasion by downregulating MMP-2 and MMP-9,up-regulating TIMP-1 and TIMP-2,and suppressing adhesion molecules.
机标关键词：
分类号：R114(卫生基础科学)
论文发表日期：2020-09-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 369-378 )
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