Oncotarget

Research Papers:

Bisphenol A deteriorates egg quality through HDAC7 suppression

Bin Liu, Shasha Zhou, Chenmin Yang, Ping Chen, Pingping Chen, Di Xi, Hong Zhu and Yuping Gao _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:92359-92365. https://doi.org/10.18632/oncotarget.21308

Metrics: PDF 1311 views  |   HTML 2541 views  |   ?  


Abstract

Bin Liu1, Shasha Zhou2, Chenmin Yang3, Ping Chen4, Pingping Chen1, Di Xi1, Hong Zhu1 and Yuping Gao1

1Department of Assisted Reproduction, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200092, People’s Republic of China

2Department of Endocrinology, Shanghai Children’s Hospital, Shanghai Jiaotong University, Shanghai 200040, People’s Republic of China

3Department of Obstetrics and Gynecology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200023, People’s Republic of China

4Institutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai 200032, People’s Republic of China

Correspondence to:

Yuping Gao, email: [email protected]

Keywords: bisphenol A, egg, HDAC7

Received: May 04, 2017    Accepted: August 26, 2017    Published: September 28, 2017

ABSTRACT

Bisphenol A (BPA), a synthetic substance of endocrine disrupter, widely distributes in environment and can affect the health of ovarian follicles, thereby impacting the fertilization ability and pregnancy rate. However, the underlying mechanisms regarding how BPA disrupts the egg quality have not been fully revealed. In this study, we determine that BPA treated female mice display the decreasing HDAC7 expression in ovary and eggs compared to control. Moreover, the global levels of H3K9 and H4K16 acetylation abnormally increase after BPA treatment and recover partially upon HDAC7 compensation. Collectively, our study reveals that BPA deteriorates egg quality through HDAC7 suppression.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 21308