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Mol. Hum. Reprod. Advance Access originally published online on June 8, 2009
Molecular Human Reproduction 2009 15(10):665-673; doi:10.1093/molehr/gap043
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© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

This article appears in the following Molecular Human Reproduction issue: Special Issue: Mechanisms of Endometriosis [View the issue table of contents]

Induction of endometrial epithelial cell invasion and c-fms expression by transforming growth factor beta

Ya-guang Liu1, Rajeshwar R. Tekmal1,2, Peter A. Binkley1, Hareesh B. Nair1,2, Robert S. Schenken1 and Nameer B. Kirma1,2,3

1Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA 2Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA

3 Correspondence address. Tel: +1 210-567-4968; Fax: +1 210-567-4958; E-mail: kirma{at}uthscsa.edu

Transforming growth factor beta 1 (TGF-β1) levels are increased in the peritoneal fluid of endometriosis patients, and endometrial cells express TGF-β signaling components; however, little is known regarding the role of TGF-β in endometriosis. Our objective was to examine the effects of TGF-β1 on (i) the expression of macrophage colony-stimulating factor receptor encoded by the c-fms gene, (ii) transmesothelial invasiveness of endometrial cells, (iii) cellular proliferation and (iv) attachment to peritoneal mesothelial cells (PMCs). Effects of TGF-β1 on c-fms mRNA expression were determined by real-time RT–PCR and c-fms cell-surface expression by flow cytometry. Effects of TGF-β1 on the invasiveness of the immortalized endometrial epithelial cell (EEC) line EM42 and primary EECs were examined using a three-dimensional in vitro system modeling the peritoneum. Cellular proliferation and attachment to PMCs were also examined using established techniques. TGF-β1 had little or no effect on cellular proliferation and endometrial cell attachment to PMCs. TGF-β1 significantly induced the expression of c-fms mRNA and c-fms cell-surface expression. TGF-β1 enhanced transmesothelial invasion by EM42 cells and EECs. Antagonists of TGF-β1 signaling significantly inhibited both the induction of c-fms expression and cellular invasiveness, suggesting that additional studies are warranted to assess the therapeutic potential of TGF-β antagonists in endometriosis.

Key words: transforming growth factor beta/c-fms/endometriosis/transmesothelial invasion/TGFBR 1 inhibitors

Submitted on March 26, 2009; resubmitted on May 26, 2009; accepted on June 3, 2009.


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