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. 2004 Dec;39(12):809-12.

[Expressions of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in ectopic and eutopic endometrium]

[Article in Chinese]
Qiong-hua Chen  1 , Jun-ying Qu, Ya-yun Xu, Na-xuan Qiu, Yan-zhen Zhuang, Shan Zhong, Qing-quan Fang
Affiliations
  • PMID: 15733405

[Expressions of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in ectopic and eutopic endometrium]

[Article in Chinese]
Qiong-hua Chen et al. Zhonghua Fu Chan Ke Za Zhi. 2004 Dec.

Abstract

Objective: To study the expression of matrix metalloproteinase-9(MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in ectopic and eutopic endometrium in patients with endometriosis.

Methods: The expressions of MMP-9 and TIMP-1 in ectopic and eutopic endometrium were detected by immunohistochemistry streptavidin-biotin peroxidase (SP) method in 45 patients with endometriosis (study group) and in 32 patients with uterine fibroid (control group).

Results: In the ectopic and eutopic endometrium of group and in the control group endometrium, the expression of MMP-9 was respectively 0.381, 0.336 and 0.276; the expression of TIMP-1 was respectively 0.239, 0.253, 0.267. As a result, the ratio of MMP-9/TIMP-1 in ectopic and eutopic endometrium of study group and in the control group endometrium was respectively 1.594, 1.293, 1.034. The difference of MMP-9, MMP-9/TIMP-1 in ectopic and eutopic and the control group endometrium was markedly significant (P < 0.01 or P < 0.05). The difference of the expression of TIMP-1 between ectopic and the control group endometrium was also markedly significant (P < 0.01). Higher expression of MMP-9 and lower expression of TIMP-1 in ectopic endometrium and higher expression of MMP-9 in eutopic endometrium occurred in the whole menses period, in which higher expression of MMP-9 in ectopic endometrium than in eutopic endometrium only took place in proliferative phase.

Conclusion: The change of expression of MMP-9 and TIMP-1 in ectopic endometrium may be related to the pathogenesis of endometriosis.

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