Mol. Hum. Reprod. Advance Access originally published online on July 30, 2009
Molecular Human Reproduction 2009 15(10):687-692; doi:10.1093/molehr/gap061
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
This article appears in the following Molecular Human Reproduction issue: Special Issue: Mechanisms of Endometriosis [View the issue table of contents]
Peroxisome-proliferator activator receptor-gamma activation decreases attachment of endometrial cells to peritoneal mesothelial cells in an in vitro model of the early endometriotic lesion
1Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Michigan Health System, Ann Arbor, MI 48109, USA 2Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA 3Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Wisconsin, H4/628 Clinical Science Center, 600 Highland Ave, Madison, WI 53792-3236, USA
4 Correspondence address. Tel: +1-608-263-1212; Fax: +1-608-262-9862; E-mail: lebovic{at}wisc.edu
The aim of this study was to investigate whether peroxisome proliferator-activated receptor (PPAR)-
activation has an effect on the attachment of endometrial cells to peritoneal mesothelial cells in a well-established in vitro model of the early endometriotic lesion. The endometrial epithelial cell line EM42 and mesothelial cell line LP9 were used for this study. EM42 cells, LP9 cells or both were treated with the PPAR- agonist ciglitazone (CTZ) at varying concentrations (10, 20 and 40 µM) x 48 h with subsequent co-culture of EM42 and LP9 cells. The rate of EM42 attachment and invasion through LP9 cells was then assessed and compared with control (EM42 and LP9 cells co-cultured without prior treatment with CTZ). Next, attachment of CTZ-treated and untreated EM42 cells to hyaluronic acid (HA), a cell adhesion molecule (CAM) on peritoneal mesothelial cells, were assessed. Although there was no difference in EM42 attachment when LP9 cells alone were treated with CTZ, treatment of EM42 cells with 40 µM CTZ decreased EM42 attachment to LP9 cells by 27% (P < 0.01). Treatment of both EM42 and LP9 cells with 40 µM CTZ decreased EM42 attachment to LP9 by 37% (P < 0.01). Treatment of EM42 cells with 40 µM CTZ decreased attachment to HA by 66% (P = 0.056). CTZ did not decrease invasion of EM42 cells through the LP9 monolayer. CTZ may inhibit EM42 cell proliferation. In conclusion, CTZ significantly decreased EM42 attachment to LP9 cells and HA in an in vitro model of the early endometriotic lesion.
Key words:
attachment/endometriosis/peritoneum/PPAR-/thiazolidinedione
Submitted on April 29, 2009; resubmitted on July 16, 2009; accepted on July 26, 2009.