Expression of CD44s, vascular endothelial growth factor, matrix metalloproteinase-2 and Ki-67 in peritoneal, rectovaginal and ovarian endometriosis.

Hye Ok Kim, Kim HO, Kwang Moon Yang, Yang KM, Kang IS, Inn Soo Kang, Mi Kyoung Koong, Koong MK, Hye Sun Kim, Kim HS, Zhang X, Xianglan Zhang, Kim I, Insun Kim
The Journal of reproductive medicine · 2007 · vol. 52(3) , pp. 207–13 · PMID:17465288 · W2410861784
article OA: closed CC0 ⤵ 20 in-corpus citations
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This study investigated CD44s, VEGF, MMP-2, and Ki-67 expression in peritoneal, rectovaginal, and ovarian endometriosis, finding differential expression patterns linked to lesion type and stage.

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Abstract

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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Condition tags

endometriosisbowel_endometriosis

MeSH descriptors

Endometriosis Ovarian Diseases Peritoneal Diseases Vaginal Diseases Adult Cell Division Endometriosis Endometriosis Endothelial Cells Endothelial Cells Female Gene Expression Regulation Humans Hyaluronan Receptors Hyaluronan Receptors Immunohistochemistry Ki-67 Antigen Ki-67 Antigen Matrix Metalloproteinase 2 Matrix Metalloproteinase 2

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