Establishment of the disease endometriosis requires the attachment and invasion of endometrial fragments into the peritoneal lining of the peritoneal cavity. For proper attachment and invasion to occur, the endometrial cells and mesothelial cells that line the surface of the peritoneum must interact. Previous studies by Witz et al. have shown that endometrial fragments can attach to mesothelial cells, but the mechanism by which these endometrial cells are able to invade through the mesothelial layer into the underlying peritoneum is not clear (Witz et al 1999, 2000, 2001). Mesothelial cells normally display an epithelial–like morphology, but in response to injury or inflammation they undergo epithelial to mesenchymal transition (EMT). As mesothelial cells undergo EMT, they lose expression of E-cadherin and cytokeratins, exhibit a fibroblast-like phenotype, and become more migratory and invasive. This transition results in the formation of gaps in the mesothelium and could allow attached endometrial cells to invade into the underlying peritoneum. Recent studies have reported the up-regulation of extracellular matrix metalloproteinase inducer, (EMMPRIN) as cancer cells undergo EMT (Abraham et al 2008). The goal of my research proposal is to determine whether secreted factors from uterine epithelial cells of endometrial fragments can cause epithelial to mesenchymal transition of mesothelial cells. In this study we utilized a human mesothelial cell line, LP-9, to examine the effect of EMMPRIN, and other uterine epithelial cell factors such as IL-1β, and TGF-β1 on EMT by monitoring changes in expression of N-cadherin, MMPs, cytokeratins, vimentin, and transcription factors twist and snail. Change in rate of migration was also assessed using the in vitro cell wounding assay.
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Induction of epithelial to mesenchymal transition in mesothelial cells by secreted factors from uterine epithelial cells
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