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International Journal of Endocrinology
Volume 2013, Article ID 789012, 6 pages
Research Article

Gram-Negative Bacterial Lipopolysaccharide Stimulates Activin A Secretion from Human Amniotic Epithelial Cells

1Department of Laboratory Sciences, Graduate School of Health Sciences, Gunma University, 3-39-22 Showa, Maebashi, Gunma 371-8514, Japan
2Kuki General Hospital, Kuki, Saitama 346-0021, Japan
3Miyazaki Prefectural Nobeoka Hospital, Nobeoka, Miyazaki 882-0835, Japan
4Yokota Maternity Hospital, Maebashi, Gunma 371-0031, Japan
5Department of Obstetrics and Gynecology, Graduate School of Medicine, Gunma University, 3-39-22 Showa, Maebashi, Gunma 371-8511, Japan

Received 29 April 2013; Accepted 1 July 2013

Academic Editor: Maria L. Dufau

Copyright © 2013 Yumiko Abe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Activin A is involved in inflammation. The present study was performed to clarify if lipopolysaccharide, a component of Gram-negative bacteria, stimulates activin A secretion from human amniotic epithelial cells and to determine if activin A plays a role in amnionitis. Fetal membranes were obtained during elective cesarean sections performed in full-term pregnancies of patients without systemic disease, signs of premature delivery, or fetal complications. Amniotic epithelial cells were isolated by trypsinization. The activin A concentrations in the culture media were measured by enzyme-linked immunosorbent assay, and cell proliferation was assessed by 5-bromo-2′-deoxyuridine incorporation. Amniotic epithelial cells secreted activin A in a cell density-dependent manner, and lipopolysaccharide (10 μg/mL) enhanced the secretion at each cell density. Lipopolysaccharide (10–50 μg/mL) also stimulated activin A secretion in a dose-dependent manner. Contrary to the effect of activin A secretion, lipopolysaccharide inhibited cell proliferation in amniotic epithelial cells. The present study suggests that lipopolysaccharide stimulation of activin A secretion may be a mechanism in the pathogenesis of amnionitis.