J Reprod Med 2007 Mar;52(3):207-13
Department of Obstetrics and Gynecology, Samsung Cheil Hospital and Women's Healthcare Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Objective: To understand the pathogenetic mechanisms of endometriosis by examining the expression of adhesion molecules (CD44s), angiogenic factor (VEGF) and matrix protease and to perform Ki-67 labeling for evaluation of proliferative activity.
Study Design: Twenty-nine peritoneal endometriosis lesions (9 red, 12 black and 8 white), 11 rectovaginal and 22 ovarian were obtained. Immunohistochemical staining was performed with antibodies for CD44, VEGF, MMP-2 and Ki-67.
Results: CD44s were expressed mainly in stroma and showed higher expression in glandular epithelium of peritoneal endometriosis than in rectovaginal and ovarian endometriosis. The stroma in red and white lesions showed higher MMP-2 expression than in black lesions. The stromal cells in rectovaginal endometriosis showed significantly lower expression of Ki-67 (p = 0.002) than in peritoneal and ovarian endometriosis. When endometriosis was analyzed according to the revised American Fertility Society classification, Ki-67 expression was high in glandular epithelium in stages I and II (p = 0.025), whereas MMP-2 expression in stromal cells was significantly high (p < 0.001) in stages III and IV.
Conclusion: CD44, VEGF and MMP-2 were consistently expressed in endometriotic epithelial and stromal cells. White lesions of peritoneal endometriosis should not be regarded as an inactive state, and MMP-2 in stromal cells may be responsible for the progression of endometriosis. The macroscopic appearance of endometriotic lesions should not be used as a criterion to define the degree of activity.
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