Hum. Reprod. Advance Access originally published online on June 13, 2008
Human Reproduction 2008 23(9):2104-2112; doi:10.1093/humrep/den215
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Regulation and activation of ezrin protein in endometriosis
1 Division of Reproductive Endocrinology, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06520-8063, USA 2 Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY 10016, USA
3 Correspondence address. Tel: +1-203-785-6618; E-mail: aydin.arici{at}yale.edu
BACKGROUND: Ezrin protein and its activated form phospho-ezrin play a role in cell morphology, motility and adhesiveness. In this study, we hypothesized that these proteins play a role in the pathogenesis of endometriosis by promoting adhesion and invasion of endometrial stromal cells (ESCs) in ectopic sites.
METHODS: We compared the expression of ezrin and phospho-ezrin in normal endometrium from women without endometriosis with their expression in eutopic and ectopic endometrial tissues from women with endometriosis, using immunohistochemistry and western blot analysis. Paired eutopic and ectopic endometrial tissue samples from women with endometriosis (n = 13) and normal endometrium from women without endometriosis (n = 12) were collected. Invasive potential of ESCs from each of these samples was compared using Matrigel membrane invasion assay.
RESULTS: Eutopic and ectopic endometrial tissues from women with endometriosis have higher ezrin and phospho-ezrin levels as confirmed by immunohistochemistry and western blot analysis (P < 0.05). The Matrigel membrane invasion assay revealed that ectopic ESCs have more invasive characteristics, more protrusions and higher ezrin staining than normal ESCs (P < 0.05).
CONCLUSIONS: Ezrin can be a potential marker for endometrial cell invasion and may play a role in the pathogenesis of endometriosis.
Key words: endometriosis/endometrium/ezrin/phosphoezrin
Submitted on December 16, 2007; resubmitted on May 1, 2008; accepted on May 13, 2008.
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