[Expressions of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 mRNA in endometriosis]

Abstract

Objective: To investigate mRNA expression of matrix metalloproteinase (MMP-9) and tissue inhibitor of metalloproteinase (TIMP-1) in ectopic endometriosis tissue and uterine endometrium from women with and without endometriosis.

Methods: Thirty-eight women with endometriosis (Revised American Fertility Society classification, RAFSI-IV) were selected as study group. Thirty-eight specimens of ovarian endometrioma (ovarian chocolate cysts, OCC), 16 red peritoneal endometriotic lesions (RPL), and 35 matched eutopic endometrium (Eu) were collected from them simultaneously at the time of surgery. Twenty specimens of endometrium from reproductive women undergoing laparoscopic surgery without endometriosis were obtained as control group. The mRNA expressions of MMP-9 and TIMP-1 were detected by reverse transcription polymerase chain reaction (RT-PCR).

Results: Expression of TIMP-1 mRNA was detected in all samples. The level from endometriosis patients and control group was similar (2.31 +/- 1.21, 2.40 +/- 0.89). However, ectopic endometrium expressed significantly fewer TIMP-1 mRNA (OCC 1.67 +/- 0.79, RPL 1.45 +/- 0.68) compared with eutopic endometrium from both endometriosis and endometriosis-free patients (P < 0.05). The positive expression rate of MMP-9 mRNA was not distinctively different among all samples. The density of MMP-9 mRNA expression in endometrium (0.49 +/- 0.28) from endometriosis patients was similar to that in ectopic endometriosis (OCC 0.46 +/- 0.22, RPL 0.33 +/- 0.12), but was significantly higher compared with endometrium (0.29 +/- 0.12) without endometriosis (P < 0.05).

Conclusions: An increase of MMP-9 mRNA expression of eutopic endometrium with endometriosis might enhance the endometrial implantation ability, thus facilitate the ectopic implantation of endometrium. Ectopic lesions express significantly less TIMP-1 mRNA, indicating they have increased invasive ability, which might facilitate the development of endometriosis.