Format

Send to

Choose Destination
Reprod Toxicol. 2012 Nov;34(3):317-22. doi: 10.1016/j.reprotox.2012.04.008. Epub 2012 May 5.

Bisphenol A induces corticotropin-releasing hormone expression in the placental cells JEG-3.

Author information

1
Biochemistry Programme, School of Life Sciences, The Chinese University of Hong Kong, Shatin, NT, Hong Kong.

Abstract

Bisphenol A is utilized to make polycarbonate plastics and is an environmental pollutant. Recent research has indicated that it is an endocrine disruptor and may interfere with reproduction. Placental corticotrophin-releasing hormone (CRH) is a peptide hormone which is involved in fetal development. Increased plasma CRH is associated with elevated risk of premature delivery. In the present study, we demonstrated that bisphenol A increased CRH mRNA expression in the placental JEG-3 cells at or above 25μM. Reporter gene assay also demonstrated that bisphenol A could induce CRH gene transactivity. Since cyclic AMP response element (CRE) is a major regulatory element located in CRH promoter, the sequence-specific binding activity was investigated by using electrophoretic mobility shift assay. Our data indicated that bisphenol A increased the CRE binding activity. Western analysis further illustrated that PKA could be the signal triggering the CRE binding and CRH gene transactivation. In summary, the present study demonstrated that bisphenol A could induce CRH expression in placental cells and the underlying signal transduction pathway was also described.

PMID:
22564983
DOI:
10.1016/j.reprotox.2012.04.008
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center