Mol. Hum. Reprod. Advance Access published online on March 21, 2008
Molecular Human Reproduction, doi:10.1093/molehr/gan016
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Activin A increases invasiveness of endometrial cells in an in-vitro model of human peritoneum
1Department of Obstetrics and Gynecology, University of Texas Health Science Center, San Antonio, TX, USA 2Departments of Obstetrics & Gynecology and Physiology, University of Minas Gerais, Belo Horizonte, Brazil 3Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Siena, Italy
Correspondence: Fernando M. Reis, MD, PhD Department of Obstetrics and Gynecology, UFMG Av. Alfredo Balena 110 – 9o andar 30130-100 Belo Horizonte, MG, Brazil Tel: (55-31) 3248-9485 Fax: (55-31) 3248-9299 e-mail: reis{at}medicina.ufmg.br
The aim of this study was to investigate whether activin A has an effect on the attachment and/or invasion of endometrial cells in a modeled peritoneum in vitro. Cultured endometrial stromal and epithelial cells were treated with activin A (6.25 to 50 ng/ml) and with activin A (25 ng/ml) with and without inhibin A or follistatin. Fluorescent labeled cells were added to confluent peritoneal mesothelial cells (PMCs) and to a monolayer of confluent PMCs grown in a MatrigelTM invasion assay. The rate of endometrial cell attachment and invasion through PMCs was assessed. The expression of cell adhesion proteins N-cadherin and E-cadherin was evaluated with real time reverse transcription PCR. Activin A (25 ng/ml) promoted invasion of the endometrial cells through the modeled peritoneum (>2.fold vs. control) and this effect was partially reversed by inhibin A and follistatin. Activin A had no effect on the rate of attachment of the endometrial cells to the PMCs or in the rate of proliferation. In addition, activin A induced a decreased mRNA expression of E-cadherin in cultured endometrial epithelial cells. In conclusion, activin A increases invasion of endometrial epithelial cells and endometrial stromal cells into modeled peritoneum. In endometrial epithelial cells, this effect may be related to down-regulation of E-cadherin expression. Further studies are warranted to evaluate the role of activin-A in the genesis of the endometriotic lesion.
Key Words: activin A/inhibin A/follistatin/endometriosis/cadherins
Presented, in part, at the 62nd Annual Meeting of the American Society for Reproductive Medicine, New Orleans, October 2006.
Submitted on January 7, 2008; resubmitted on March 3, 2008; accepted on March 5, 2008.
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