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Mol. Hum. Reprod. Advance Access published online on June 8, 2009
Molecular Human Reproduction, 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

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,*

2Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio 2Cancer Therapy and Research Center, San Antonio, Texas, 78229, USA

* Corresponding Author: NB Kirma, Department of Obstetrics and Gynecology, 7703 Floyd Curl Drive, University of Texas Health Science Centre at San Antonio, TX 78229 Phone: 210-567-4968; Fax: 210-567-4958; E-mail: kirma{at}uthscsa.edu. Reprint requests should be addressed to NB Kirma

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 1) the expression of macrophage colony-stimulating factor receptor encoded by the c-fms gene, 2) trans-mesothelial invasiveness of endometrial cells, 3) cellular proliferation and 4) 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 trans-mesothelial 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

Abbreviated Title: TGF-beta in endometriosis

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


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[Abstract] [Full Text] [PDF]


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