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Reproductive Endocrinology and Cell Signaling Laboratory (S.K.B., J.L., J.A.A.), Department of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas 77843; Division of Anatomic Pathology (V.O.S.), Department of Pathology, Scott & White Memorial Hospital, Texas A&M University Health Science Center, Temple, Texas 76508; and Molekulare Zellbiologie und Humangenetik (A.S.-P.), Institut für Zellbiologie und Neurowissenschaft, Johann Wolfgang Goethe-Universität, 60323 Frankfurt am Main, Germany
Address all correspondence and requests for reprints to: Joe A. Arosh, Ph.D., Department of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Mail Stop TAMU 4458, Texas A&M University, College Station, Texas 77843. E-mail: jarosh{at}cvm.tamu.edu.
Endometriosis is a debilitating disease characterized by the presence of functional endometrial glandular epithelium and stroma outside the uterine cavity that affects up to 20% of women of child-bearing age. Cyclooxygenase-2 (COX-2), a rate-limiting enzyme in the biosynthesis of prostaglandin E2 (PGE2), is highly expressed in endometriotic tissues and results in increased concentrations of peritoneal PGE2 in women. In this study, we determined the expression of COX-2 protein in ectopic and eutopic endometria in humans and the role of COX-2 in endometriotic cell survival, migration, and invasion in humans. Our results indicate that COX-2 protein is abundantly expressed in ectopic endometria compared with eutopic endometria. Comparatively, expression of COX-2 protein is higher in eutopic endometria from women with endometriosis compared with women without endometriosis. Inhibition of COX-2 decreases survival, migration, and invasion of endometriotic cells that are associated with decreased production of PGE2. Cell growth inhibitory effects of COX-2 inhibition/silencing are mediated through nuclear poly (ADP-ribose) polymerase-mediated apoptosis. Cell motility and invasion inhibitory effects of COX-2 inhibition/silencing are mediated through matrix metalloproteinase-2 and -9 activities. Interestingly, effects of COX-2 inhibition is more profound in endometriotic epithelial than in stromal cells. Furthermore, inhibition of COX-2 affects invasion rather than migration of endometriotic epithelial and stromal cells. It is the first evidence showing that inhibition of COX-2 decreases endometriotic epithelial and stromal cell survival, migration, and invasion in humans. Our results support the emerging concept that COX-2/PGE2 promotes the pathophysiology and pathogenesis of endometriosis in humans.
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