Expression of matrix metalloproteinases in ovarian endometriomas: immunohistochemical study and enzyme immunoassay

被引:109
作者
Mizumoto, H [1 ]
Saito, T [1 ]
Ashihara, K [1 ]
Nishimura, M [1 ]
Takehara, M [1 ]
Tanaka, R [1 ]
Ito, E [1 ]
Kudo, R [1 ]
机构
[1] Sapporo Med Univ, Dept Obstet & Gynecol, Sch Med, Chuo Ku, Sapporo, Hokkaido 0600061, Japan
关键词
endometriosis; endometrioma; MMP; menstrual cycle; immunohistochemistry;
D O I
10.1016/S0024-3205(02)01641-7
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
Like carcinoma, endometriosis has the unique characteristics, of invasion and metastasis, though pathologically, it is a benign tumor. However, the mechanism of destruction of the surrounding tissue in endometriosis is still unclear. In this study, the expression and localization of matrix metalloproteinases (MMP)-1, -2, -3, -7, -9 and tissue inhibitors of metalloprotemases-1 (TIMP-1) were evaluated by immunohistochemistry for 20 cases and the amounts of MMP-1, TIMP-1 and MMP-1/TIMP-1 complex in the fluid of endometrioma, were analyzed by ELISA and western blotting for 20 cases, which were analyzed by immunohistochemical study. MMP-1, -2 and -9 were detected strongly in both stromal and epithelial cells and MMP-7 in the epithelial cells in the menstrual period. MMP-3 was mainly expressed in macrophage containing hemosiderin but the change of expression was not clear. TIMP-1 was intensively detected in both stromal and epithelial cells in the menstrual period but the expression decreased in other stages of the menstrual cycle. ELISA for MMP-1 also showed results similar to immunohistochemistry, suggesting that it was released to the cyst in the menstrual period when it was released to the extracellular space from the cytoplasm. The expression of TIMP-I was not clearly changed during the menstrual cycle. From these results, it was suggested that the destruction of the surrounding matrix by endometriosis might be caused by various MMPs, which are mainly produced in stromal cells. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:259 / 273
页数:15
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