Activin A increases invasiveness of endometrial cells in an in vitro model of human peritoneum

Márcia Cristina França Ferreira, Craig A. Witz, L S Hammes, Nameer B. Kirma, Felice Petraglia, Robert S. Schenken, Fernando M. Reis
In: Molecular Human Reproduction · 2008 · vol. 14(5) , pp. 301–307 · doi:10.1093/molehr/gan016 · PMID:18359784 · W2106578670
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Activin A increased endometrial cell invasion through a modeled human peritoneum in vitro, potentially by down-regulating E-cadherin expression.

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Abstract

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 cells (ESCs) and endometrial epithelial cells (EECs) were treated with activin A (6.25-50 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 Matrigel invasion assay. The rate of endometrial cell attachment and invasion through PMCs was assessed. The expression of cell adhesion proteins N- and E-cadherin was evaluated with real-time RT-PCR. Activin A (25 ng/ml) promoted invasion of the endometrial cells through the modeled peritoneum (>2-fold versus 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 EECs. In conclusion, activin A increases invasion of EECs and ESCs into modeled peritoneum. In EECs, 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.

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