基质金属蛋白酶9及其组织抑制剂1在子宫内膜异位症组织中的表达

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

目的探讨基质金属蛋白酶9(MMP-9)及其组织抑制剂1(TTMP-1)在子宫内膜异位症(内异症)患者异位内膜及在位内膜中的表达,及其在内异症发病中的作用。方法选取38例根据美国生育学会修订的内异症分期法,诊断为内异症患者的卵巢内膜异位囊肿标本38份、腹膜红色病变标本16份及同期在位内膜35份组织作为研究组,以及非内异症患者的子宫内膜标本20份作为对照组。采用RT-PCR半定量技术,检测上述不同组织中MMP-9mRNA及TIMP-1mRNA的表达率及表达强度。结果两组所有标本均有TIMP-1mRNA表达,部分标本有MMP-9mRNA表达。研究组中,卵巢异位囊肿及腹膜红色病变组织MMP-9mRNA表达率分别为45%及56%,表达强度分别为0·46±0·22及0·33±0·12;同期在位内膜MMP-9mRNA表达率为57%,表达强度为0·49±0·28。卵巢异位囊肿、腹膜红色病变及同期在位内膜组织TIMP-1mRNA表达强度分别为1·67±0·79、1·45±0·68及2·31±1·21,前两者与后者比较,差异有统计学意义(P<0·05)。研究组在位内膜及对照组MMP-9的表达率分别为57%及45%;表达强度分别为0·49±0·28及0·29±0·12,两组比较,差异有统计学意义(P<0·05)。研究组在位内膜及对照组TIMP-1mRNA的表达强度分别为2·31±1·21及2·40±0·89。结论内异症患者在位内膜MMP-9mRNA的表达增强,促进了内膜的异位种植。异位内膜TIMP-1mRNA的表达减弱,可促使内异症病变的发展。

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, RAFS Ⅰ -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.